The document discusses the Paramyxoviridae family of viruses. It belongs to the order Mononegavirales and includes enveloped viruses with negative-sense single-stranded RNA genomes. The family is divided into two subfamilies and several genera. Key characteristics include virion morphology, genome organization, and viral proteins. Notable members that cause disease in animals are bovine parainfluenza virus 3 and avian paramyxovirus type 1 viruses (which include Newcastle disease virus). Clinical signs and epidemiology of infections are described.
Parvo virus is a highly contagious virus that mainly affects dogs. It spreads between dogs through contact with their feces. Vaccines can prevent infection but mortality reaches 91% in untreated cases. Parvo virus causes vomiting, diarrhea, and leukopenia in infected dogs. It replicates in actively dividing cells and is shed in feces, vomit, urine, and saliva, making it very stable in the environment.
This document discusses RNA viruses, specifically influenza viruses and paramyxoviruses. It provides classifications of RNA viruses including families such as Orthomyxoviridae, Paramyxoviridae, Coronaviridae, and Retroviridae. Details are given on the structure, replication, and transmission of influenza viruses and paramyxoviruses. The clinical features, diagnosis, treatment and prevention of influenza and specific paramyxoviruses like mumps are summarized.
Rabies virus belongs to the family Rhabdoviridae and causes an estimated 55,000 human deaths worldwide each year. Rabies virus is transmitted primarily through bites from infected carnivores and bats. After entering the body through a bite, the virus travels along nerve cells to the brain, where it causes an encephalitis and eventual death if not treated promptly. Symptoms progress from pain or itching at the bite site to neurological symptoms such as fear of water, seizures, and paralysis.
A detailed description of HIV covering virology, morphology, pathogenesis, clinical stages and manifestations, laboratory diagnosis, and diagnostic strategy, and therapeutic options and prevention.
Viruses and prions are two types of infectious agents. Viruses are small microorganisms that infect other living organisms and consist of nucleic acid surrounded by a protein shell. They can cause oral diseases. Prions are proteinaceous particles that can self-replicate and induce neurodegenerative diseases like Creutzfeldt-Jakob disease in humans after a long incubation period. They are highly resistant to inactivation.
Viruses are microscopic particles that infect cells and rely on host cells to replicate. They contain genetic material in the form of DNA or RNA and have a protein coat. Viruses infect both eukaryotic and prokaryotic cells and differ from other organisms in their structure, biology, and reproduction. Viruses are classified into groups based on their structure and method of replication, with the Baltimore system categorizing viruses into 7 groups depending on their nucleic acid and method of replication.
Rabies virus causes a fatal viral infection of the central nervous system called rabies encephalitis. It is transmitted via saliva and has an incubation period of 20-90 days. The bullet-shaped virus contains a single-stranded RNA genome and enters cells via endocytosis, where it replicates and produces new viral particles that bud from the cell. The G protein mediates viral attachment and elicits protective neutralizing antibodies. While nucleoprotein antibodies are diagnostic, only neutralizing antibodies against the G protein provide protection against rabies infection.
Viruses are biological agents that reproduce inside host cells. They contain genetic material in the form of DNA or RNA and a protein coat. Viruses come in various shapes and sizes, and there are over 2,000 known virus species that can infect humans and cause diseases like influenza, hepatitis C, and SARS. Viruses have a life cycle where they attach and penetrate a host cell, use the cell to replicate their genetic material and proteins, assemble new virus particles, and are released to infect new cells. Viruses are classified based on their genetic material and structure. Important human virus families include those with RNA genomes like influenza virus and those with DNA genomes like adenovirus.
Parvo virus is a highly contagious virus that mainly affects dogs. It spreads between dogs through contact with their feces. Vaccines can prevent infection but mortality reaches 91% in untreated cases. Parvo virus causes vomiting, diarrhea, and leukopenia in infected dogs. It replicates in actively dividing cells and is shed in feces, vomit, urine, and saliva, making it very stable in the environment.
This document discusses RNA viruses, specifically influenza viruses and paramyxoviruses. It provides classifications of RNA viruses including families such as Orthomyxoviridae, Paramyxoviridae, Coronaviridae, and Retroviridae. Details are given on the structure, replication, and transmission of influenza viruses and paramyxoviruses. The clinical features, diagnosis, treatment and prevention of influenza and specific paramyxoviruses like mumps are summarized.
Rabies virus belongs to the family Rhabdoviridae and causes an estimated 55,000 human deaths worldwide each year. Rabies virus is transmitted primarily through bites from infected carnivores and bats. After entering the body through a bite, the virus travels along nerve cells to the brain, where it causes an encephalitis and eventual death if not treated promptly. Symptoms progress from pain or itching at the bite site to neurological symptoms such as fear of water, seizures, and paralysis.
A detailed description of HIV covering virology, morphology, pathogenesis, clinical stages and manifestations, laboratory diagnosis, and diagnostic strategy, and therapeutic options and prevention.
Viruses and prions are two types of infectious agents. Viruses are small microorganisms that infect other living organisms and consist of nucleic acid surrounded by a protein shell. They can cause oral diseases. Prions are proteinaceous particles that can self-replicate and induce neurodegenerative diseases like Creutzfeldt-Jakob disease in humans after a long incubation period. They are highly resistant to inactivation.
Viruses are microscopic particles that infect cells and rely on host cells to replicate. They contain genetic material in the form of DNA or RNA and have a protein coat. Viruses infect both eukaryotic and prokaryotic cells and differ from other organisms in their structure, biology, and reproduction. Viruses are classified into groups based on their structure and method of replication, with the Baltimore system categorizing viruses into 7 groups depending on their nucleic acid and method of replication.
Rabies virus causes a fatal viral infection of the central nervous system called rabies encephalitis. It is transmitted via saliva and has an incubation period of 20-90 days. The bullet-shaped virus contains a single-stranded RNA genome and enters cells via endocytosis, where it replicates and produces new viral particles that bud from the cell. The G protein mediates viral attachment and elicits protective neutralizing antibodies. While nucleoprotein antibodies are diagnostic, only neutralizing antibodies against the G protein provide protection against rabies infection.
Viruses are biological agents that reproduce inside host cells. They contain genetic material in the form of DNA or RNA and a protein coat. Viruses come in various shapes and sizes, and there are over 2,000 known virus species that can infect humans and cause diseases like influenza, hepatitis C, and SARS. Viruses have a life cycle where they attach and penetrate a host cell, use the cell to replicate their genetic material and proteins, assemble new virus particles, and are released to infect new cells. Viruses are classified based on their genetic material and structure. Important human virus families include those with RNA genomes like influenza virus and those with DNA genomes like adenovirus.
This document provides an overview of influenza viruses. It discusses that influenza viruses are a major cause of respiratory disease worldwide and have caused millions of deaths. It describes the three types of influenza viruses (A, B, C), their structures, proteins, replication cycles, mechanisms of antigenic drift and shift, and pathogenesis. The document also covers epidemiology, prevention strategies like vaccines and antiviral drugs, and treatment of influenza.
Ques-7Viruses contain DNA (deoxyribonucleic acid) or RNA (ribonuc.pdfaquacare2008
Ques-7:
Viruses contain DNA (deoxyribonucleic acid) or RNA (ribonucleic acid) as their genetic
material, and they reproduce in the host cells. Bacteriophage is a type of virus that can infect
bacteria and inject its genome into the host, the bacteria then produces dozens of viral lineages.
Retrovirus such as HIV (human immune deficiency virus) reproduces in a different way, as they
contain reverse transcriptase enzyme. In this, a complementary DNA is transcribed from the
RNA genome, and it is called as DNA provirus.
The rate of evolution in RNA-based viruses (microcosm), like HIV-1 has million times higher
mutation rate when compared to that of DNA-based organisms (bacteria humans etc). It can
rapidly changes its genome components under biological conditions to acquire adaptations for
survival (resistance against drugs, immune components) in the biological host cell medium
compared to the DNA based organisms in which lower rate of evolutionary adaptations were
observed. This property of high genomic mutation rate in HIV-1 retrovirus is due to the
following mechanisms.
Viral genome transcribe via reverse transcription finally proved HIV-1 mRNA (after splicing)
with Rev 350 nucleotide sequences. These Rev produced once the viral mRNA transferred to the
cytoplasm from the nucleus for translation. Virulence is the factor of causing extensive damage
to the host cell and infecting new host cell in which pathogen is going to undergo extensive rate
of reproduction & phase variation along with genome modification to defend host immune
system. This is the main basis of evolution and an example ahs described below.
Several mutated viral lineages are produced due to the nucleotide integration into the host cells
& change their genome finally code for the enzymatic proteins such as reverse transcriptase,
ribonuclease, and integrase in order to promote severe multiplication of integrated host genome
with viral protein predominanlty result in several lineages (multiple capies of virions).
For example: Viral evolution mechanism with new genome & producetion of several viral
lineages
1. After viral particle entry, viral genome integrates into the host cell genome and replicate
followed by expression. Later the novel synthesized viral proteins are going to be transported to
specific sites for assembly into progeny virus thereby-----> more assembly/progeny
2. Even though viral assembly is going to takes place in the host cell plasma membrane, but a
variety of viral genomes initiate assembly in intracellular organelles or nucleus predominantly.
Thereby further particle/plaque forming units associate with exocytosis of the viral and host cell
integrated genome after lysis. Finally again mature viral lineages are going to target new cells.
Reverse transcriptase induced complementary DNA synthesis followed by mRNA synthesis for
viral protein -coding repoitre. This enzyme enables to produce more viral genome particle by
integrating into the host cell followed by vir.
Viruses are small obligate intracellular parasites, which by definition contain either a RNA or DNA genome surrounded by a protective, virus-coded protein coat. Viruses range from the
structurally simple and small parvoviruses and picornaviruses to the large and complex
poxviruses and herpesviruses. Viruses are classified on the basis of morphology, chemical
composition, and mode of replication. The viruses that infect humans are currently grouped into 21 families, reflecting only a small part of the spectrum of the multitude of different viruses whose host ranges extend from vertebrates to protozoa and from plants and fungi to bacteria.
Viruses are small obligate intracellular parasites, which by definition contain either an RNA or DNA genome surrounded by a protective, virus-coded protein coat. Viruses range from the structurally simple and small parvoviruses and picornaviruses to the large and complex poxviruses and herpesviruses. Viruses are classified on the basis of morphology, chemical composition, and mode of replication. The viruses that infect humans are currently grouped into 21 families, reflecting only a small part of the spectrum of the multitude of different viruses whose host ranges extend from vertebrates to protozoa and from plants and fungi to bacteria.
This document discusses virus classification systems. It provides an overview of the Baltimore classification system, which categorizes viruses based on their method of mRNA production. Group I viruses contain double-stranded DNA and produce mRNA through transcription. Group II viruses have single-stranded DNA and produce a double-stranded DNA intermediate before transcription. Group III viruses use double-stranded RNA, with one strand serving as the mRNA template. Group IV viruses contain single-stranded RNA with positive polarity that directly serves as mRNA.
1) Coronaviridae is a family of enveloped, positive-stranded RNA viruses which infect amphibians, birds and mammals. They were recognized as a new virus family in 1968.
2) Coronaviruses have large club-shaped spikes and a genome consisting of the largest known non-segmented RNA. They utilize a distinctive nested set transcription strategy.
3) Viral replication occurs within an extensive membranous network, utilizing a complex strategy of full-length genomic RNA synthesis and a nested set of subgenomic mRNAs. This allows expression of downstream genes and leads to genetic diversity through recombination.
Viruses are complexes consisting of protein and an RNA or DNA genome that lack cellular structure and independent metabolism. They replicate solely by exploiting living cells based on the information in their genome. Viruses come in a variety of sizes and structures, and can have DNA or RNA genomes. They reproduce by first binding to and entering a host cell, then exploiting the cell's machinery to produce new viral components and assemble new virus particles, which then burst out to infect other cells. Viruses are classified based on properties like their genome, capsid symmetry, presence of an envelope, and more. While they cannot be treated with antibiotics, some antiviral drugs can inhibit specific stages of the viral replication process.
Viral replication involves three main stages: early events of adsorption, penetration and uncoating; middle events of transcription, translation and genome replication; and late events of assembly, release and lysis. The viral growth curve shows an eclipse period when no virus is detectable followed by a latent period until new virus appears and causes cytopathic effects. RNA viruses use different strategies to synthesize mRNA depending on whether their genome is single- or double-stranded and positive or negative sense. Viruses can also enter a lysogenic cycle where the viral DNA integrates into the host genome until induced to enter the lytic cycle.
Bunyaviridae is a large family of viruses that includes over 300 species. They have a spherical virion measuring 90-100nm with three segments of negative sense RNA and a helical nucleocapsid. Bunyaviruses are transmitted by arthropods like mosquitoes and ticks or through inhalation of aerosols from infected rodents. They cause diseases in humans ranging from febrile illnesses to viral hemorrhagic fevers. Diagnosis involves serology, virus isolation, PCR and observing the geographic location and season of exposure. Prevention strategies include vaccines, controlling vector populations, personal protective measures and rodent control.
The document discusses different types of infectious agents including viruses, viroids, virusoids, and prions. It describes their structures and compositions. Viruses are obligate intracellular parasites that contain their own genome and proteins. Viroids contain only RNA, virusoids contain nucleic acid and a virus capsid, and prions are composed solely of protein. Defective viruses also require a helper virus. The document then discusses the history of virology discoveries and provides comparisons of viruses and cells.
The document summarizes key aspects of virology. It describes that viruses are small infectious agents that contain either DNA or RNA and use the machinery of host cells to replicate. Viruses infect cells and program them to produce new viral components for assembly of new virus particles. The document then discusses viral structure, morphology, replication cycles involving attachment, entry, uncoating, production of components, assembly and release. It also covers pathogenesis, diagnosis, cultivation, and methods for prevention and treatment of viral infections including vaccines, interferons and antiviral drugs.
Infectious laryngotracheitis is a highly contagious respiratory disease of chickens and pheasants caused by gallid herpesvirus 1. The virus infects the upper respiratory tract, causing swelling and the production of bloody mucus. Clinical signs range from mild illness to high mortality depending on the strain. The virus establishes latency in trigeminal ganglia. Diagnosis involves detecting viral antigens or DNA in samples. Vaccines include live-attenuated and inactivated versions. Prevention relies on vaccination programs, biosecurity, and cleaning between flocks.
Virology is the study of viruses and their relationship with hosts. Viruses are acellular organisms that can only replicate inside host cells. They have nucleic acid genomes and use host cell machinery to assemble new viral particles. Viruses come in a variety of shapes and sizes, and some have envelopes derived from host cell membranes. They enter host cells, express their genes, replicate their genomes, assemble new viral particles, and exit host cells to infect new targets. Viruses are cultivated using various methods including cell cultures, embryonated eggs, and animal models to study viral replication and pathogenesis.
viral taxonomy,classification and properties.pptxdrnehami
Viruses are the smallest infectious agents that can only replicate inside living cells. They contain nucleic acid, either DNA or RNA, encased within a protein shell called a capsid. Some viruses have an outer envelope as well. Viruses infect cells by binding to specific receptors on the host cell and introducing their genetic material. Inside the cell, viruses use the host cell's machinery to produce new virus particles that are then released to infect other cells. Viruses are classified based on properties like morphology, genome type, replication strategy, and antigenic characteristics. Major virus families include DNA viruses like herpesviruses, adenoviruses and parvoviruses, and RNA viruses like picornaviruses, flavivir
Viruses are non-living agents that infect all life forms and are obligate intracellular parasites. They contain either DNA or RNA and have a protein coat called a capsid that is sometimes enclosed in an envelope. Viruses have a specific host range determined by attachment sites and cellular factors, and they replicate either through a lytic cycle that ends in host cell lysis or a lysogenic cycle where the host cell remains alive. Bacteriophages in particular can undergo lytic cycles involving attachment, penetration, biosynthesis, maturation and release steps or lysogenic cycles where the phage DNA is incorporated into the host genome.
Retroviruses can be used as tools in cell biology. They contain an RNA genome and reverse transcriptase enzyme, which allows them to insert their DNA into the host cell genome. Their life cycle involves reverse transcribing their RNA into DNA within the cell. This proviral DNA may then remain latent or produce new viral particles. Retroviral vectors can be engineered to express genes of interest by removing viral genes and adding the gene of interest, allowing them to integrate and persist long-term in infected cells. These vectors have been used to label and study tumor cells, brain development, and the effects of gene expression.
Viruses are obligate intracellular parasites that rely on host cell synthetic processes for replication. Effective antiviral agents must block viral entry/exit from cells or be active inside host cells. They inhibit virus-specific replication events or preferentially inhibit virus-directed nucleic acid or protein synthesis over host-directed synthesis. Targets include viral DNA/RNA synthesis and structural/enzymatic proteins. Common antiviral drug classes inhibit viral entry, reverse transcription, protease activity, and more. Side effects depend on drug class but can include liver toxicity, hematological abnormalities, and more.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
This document provides an overview of influenza viruses. It discusses that influenza viruses are a major cause of respiratory disease worldwide and have caused millions of deaths. It describes the three types of influenza viruses (A, B, C), their structures, proteins, replication cycles, mechanisms of antigenic drift and shift, and pathogenesis. The document also covers epidemiology, prevention strategies like vaccines and antiviral drugs, and treatment of influenza.
Ques-7Viruses contain DNA (deoxyribonucleic acid) or RNA (ribonuc.pdfaquacare2008
Ques-7:
Viruses contain DNA (deoxyribonucleic acid) or RNA (ribonucleic acid) as their genetic
material, and they reproduce in the host cells. Bacteriophage is a type of virus that can infect
bacteria and inject its genome into the host, the bacteria then produces dozens of viral lineages.
Retrovirus such as HIV (human immune deficiency virus) reproduces in a different way, as they
contain reverse transcriptase enzyme. In this, a complementary DNA is transcribed from the
RNA genome, and it is called as DNA provirus.
The rate of evolution in RNA-based viruses (microcosm), like HIV-1 has million times higher
mutation rate when compared to that of DNA-based organisms (bacteria humans etc). It can
rapidly changes its genome components under biological conditions to acquire adaptations for
survival (resistance against drugs, immune components) in the biological host cell medium
compared to the DNA based organisms in which lower rate of evolutionary adaptations were
observed. This property of high genomic mutation rate in HIV-1 retrovirus is due to the
following mechanisms.
Viral genome transcribe via reverse transcription finally proved HIV-1 mRNA (after splicing)
with Rev 350 nucleotide sequences. These Rev produced once the viral mRNA transferred to the
cytoplasm from the nucleus for translation. Virulence is the factor of causing extensive damage
to the host cell and infecting new host cell in which pathogen is going to undergo extensive rate
of reproduction & phase variation along with genome modification to defend host immune
system. This is the main basis of evolution and an example ahs described below.
Several mutated viral lineages are produced due to the nucleotide integration into the host cells
& change their genome finally code for the enzymatic proteins such as reverse transcriptase,
ribonuclease, and integrase in order to promote severe multiplication of integrated host genome
with viral protein predominanlty result in several lineages (multiple capies of virions).
For example: Viral evolution mechanism with new genome & producetion of several viral
lineages
1. After viral particle entry, viral genome integrates into the host cell genome and replicate
followed by expression. Later the novel synthesized viral proteins are going to be transported to
specific sites for assembly into progeny virus thereby-----> more assembly/progeny
2. Even though viral assembly is going to takes place in the host cell plasma membrane, but a
variety of viral genomes initiate assembly in intracellular organelles or nucleus predominantly.
Thereby further particle/plaque forming units associate with exocytosis of the viral and host cell
integrated genome after lysis. Finally again mature viral lineages are going to target new cells.
Reverse transcriptase induced complementary DNA synthesis followed by mRNA synthesis for
viral protein -coding repoitre. This enzyme enables to produce more viral genome particle by
integrating into the host cell followed by vir.
Viruses are small obligate intracellular parasites, which by definition contain either a RNA or DNA genome surrounded by a protective, virus-coded protein coat. Viruses range from the
structurally simple and small parvoviruses and picornaviruses to the large and complex
poxviruses and herpesviruses. Viruses are classified on the basis of morphology, chemical
composition, and mode of replication. The viruses that infect humans are currently grouped into 21 families, reflecting only a small part of the spectrum of the multitude of different viruses whose host ranges extend from vertebrates to protozoa and from plants and fungi to bacteria.
Viruses are small obligate intracellular parasites, which by definition contain either an RNA or DNA genome surrounded by a protective, virus-coded protein coat. Viruses range from the structurally simple and small parvoviruses and picornaviruses to the large and complex poxviruses and herpesviruses. Viruses are classified on the basis of morphology, chemical composition, and mode of replication. The viruses that infect humans are currently grouped into 21 families, reflecting only a small part of the spectrum of the multitude of different viruses whose host ranges extend from vertebrates to protozoa and from plants and fungi to bacteria.
This document discusses virus classification systems. It provides an overview of the Baltimore classification system, which categorizes viruses based on their method of mRNA production. Group I viruses contain double-stranded DNA and produce mRNA through transcription. Group II viruses have single-stranded DNA and produce a double-stranded DNA intermediate before transcription. Group III viruses use double-stranded RNA, with one strand serving as the mRNA template. Group IV viruses contain single-stranded RNA with positive polarity that directly serves as mRNA.
1) Coronaviridae is a family of enveloped, positive-stranded RNA viruses which infect amphibians, birds and mammals. They were recognized as a new virus family in 1968.
2) Coronaviruses have large club-shaped spikes and a genome consisting of the largest known non-segmented RNA. They utilize a distinctive nested set transcription strategy.
3) Viral replication occurs within an extensive membranous network, utilizing a complex strategy of full-length genomic RNA synthesis and a nested set of subgenomic mRNAs. This allows expression of downstream genes and leads to genetic diversity through recombination.
Viruses are complexes consisting of protein and an RNA or DNA genome that lack cellular structure and independent metabolism. They replicate solely by exploiting living cells based on the information in their genome. Viruses come in a variety of sizes and structures, and can have DNA or RNA genomes. They reproduce by first binding to and entering a host cell, then exploiting the cell's machinery to produce new viral components and assemble new virus particles, which then burst out to infect other cells. Viruses are classified based on properties like their genome, capsid symmetry, presence of an envelope, and more. While they cannot be treated with antibiotics, some antiviral drugs can inhibit specific stages of the viral replication process.
Viral replication involves three main stages: early events of adsorption, penetration and uncoating; middle events of transcription, translation and genome replication; and late events of assembly, release and lysis. The viral growth curve shows an eclipse period when no virus is detectable followed by a latent period until new virus appears and causes cytopathic effects. RNA viruses use different strategies to synthesize mRNA depending on whether their genome is single- or double-stranded and positive or negative sense. Viruses can also enter a lysogenic cycle where the viral DNA integrates into the host genome until induced to enter the lytic cycle.
Bunyaviridae is a large family of viruses that includes over 300 species. They have a spherical virion measuring 90-100nm with three segments of negative sense RNA and a helical nucleocapsid. Bunyaviruses are transmitted by arthropods like mosquitoes and ticks or through inhalation of aerosols from infected rodents. They cause diseases in humans ranging from febrile illnesses to viral hemorrhagic fevers. Diagnosis involves serology, virus isolation, PCR and observing the geographic location and season of exposure. Prevention strategies include vaccines, controlling vector populations, personal protective measures and rodent control.
The document discusses different types of infectious agents including viruses, viroids, virusoids, and prions. It describes their structures and compositions. Viruses are obligate intracellular parasites that contain their own genome and proteins. Viroids contain only RNA, virusoids contain nucleic acid and a virus capsid, and prions are composed solely of protein. Defective viruses also require a helper virus. The document then discusses the history of virology discoveries and provides comparisons of viruses and cells.
The document summarizes key aspects of virology. It describes that viruses are small infectious agents that contain either DNA or RNA and use the machinery of host cells to replicate. Viruses infect cells and program them to produce new viral components for assembly of new virus particles. The document then discusses viral structure, morphology, replication cycles involving attachment, entry, uncoating, production of components, assembly and release. It also covers pathogenesis, diagnosis, cultivation, and methods for prevention and treatment of viral infections including vaccines, interferons and antiviral drugs.
Infectious laryngotracheitis is a highly contagious respiratory disease of chickens and pheasants caused by gallid herpesvirus 1. The virus infects the upper respiratory tract, causing swelling and the production of bloody mucus. Clinical signs range from mild illness to high mortality depending on the strain. The virus establishes latency in trigeminal ganglia. Diagnosis involves detecting viral antigens or DNA in samples. Vaccines include live-attenuated and inactivated versions. Prevention relies on vaccination programs, biosecurity, and cleaning between flocks.
Virology is the study of viruses and their relationship with hosts. Viruses are acellular organisms that can only replicate inside host cells. They have nucleic acid genomes and use host cell machinery to assemble new viral particles. Viruses come in a variety of shapes and sizes, and some have envelopes derived from host cell membranes. They enter host cells, express their genes, replicate their genomes, assemble new viral particles, and exit host cells to infect new targets. Viruses are cultivated using various methods including cell cultures, embryonated eggs, and animal models to study viral replication and pathogenesis.
viral taxonomy,classification and properties.pptxdrnehami
Viruses are the smallest infectious agents that can only replicate inside living cells. They contain nucleic acid, either DNA or RNA, encased within a protein shell called a capsid. Some viruses have an outer envelope as well. Viruses infect cells by binding to specific receptors on the host cell and introducing their genetic material. Inside the cell, viruses use the host cell's machinery to produce new virus particles that are then released to infect other cells. Viruses are classified based on properties like morphology, genome type, replication strategy, and antigenic characteristics. Major virus families include DNA viruses like herpesviruses, adenoviruses and parvoviruses, and RNA viruses like picornaviruses, flavivir
Viruses are non-living agents that infect all life forms and are obligate intracellular parasites. They contain either DNA or RNA and have a protein coat called a capsid that is sometimes enclosed in an envelope. Viruses have a specific host range determined by attachment sites and cellular factors, and they replicate either through a lytic cycle that ends in host cell lysis or a lysogenic cycle where the host cell remains alive. Bacteriophages in particular can undergo lytic cycles involving attachment, penetration, biosynthesis, maturation and release steps or lysogenic cycles where the phage DNA is incorporated into the host genome.
Retroviruses can be used as tools in cell biology. They contain an RNA genome and reverse transcriptase enzyme, which allows them to insert their DNA into the host cell genome. Their life cycle involves reverse transcribing their RNA into DNA within the cell. This proviral DNA may then remain latent or produce new viral particles. Retroviral vectors can be engineered to express genes of interest by removing viral genes and adding the gene of interest, allowing them to integrate and persist long-term in infected cells. These vectors have been used to label and study tumor cells, brain development, and the effects of gene expression.
Viruses are obligate intracellular parasites that rely on host cell synthetic processes for replication. Effective antiviral agents must block viral entry/exit from cells or be active inside host cells. They inhibit virus-specific replication events or preferentially inhibit virus-directed nucleic acid or protein synthesis over host-directed synthesis. Targets include viral DNA/RNA synthesis and structural/enzymatic proteins. Common antiviral drug classes inhibit viral entry, reverse transcription, protease activity, and more. Side effects depend on drug class but can include liver toxicity, hematological abnormalities, and more.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
2. Family Paramyxoviridae is included in the order Mononegavirales,
along with families Rhabdoviridae, Filoviridae, & Bornaviridae
All these viruses are enveloped &, other than bornaviruses, have
prominent envelope glycoprotein spikes
All viruses included in the order have genomes consisting of single
molecule of negative-sense, single-stranded RNA
PROPERTIES OF PARAMYXOVIRUSES
Classification
Family Paramyxoviridae is subdivided into subfamilies
Paramyxovirinae & Pneumovirinae, former having genera Respirovirus,
Avulavirus, Henipavirus, Rubulavirus, & Morbillivirus
latter genera - Pneumovirus & Metapneumovirus
4. Nomenclature of viruses within the family Paramyxoviridae is
confusing & fraught with inconsistencies, as individual viruses have
variously named according to their species of origin
(e.g., porcine rubulavirus, avian paramyxoviruses 2–9)
geographic sites of discovery (e.g., Sendai, Hendra, & Newcastle
disease viruses)
antigenic relationships (e.g., human parainfluenza viruses 1–4)
or given names related to the diseases that they produce in affected
animals or humans (e.g., canine distemper, rinderpest, measles, &
mumps viruses)
VIRION PROPERTIES
Paramyxovirus virions are pleomorphic (spherical as well as
filamentous forms occur), 150–350 nm in diameter
5. Virions are enveloped, covered with large glycoprotein spikes (8–14 nm in
length), & contain a “herringbone-shaped” helically symmetrical
nucleocapsid, 1 µm in length & 18 nm (Paramyxovirinae) or 13–14 nm
(Pneumovirinae) in diameter
Genome consists of a single linear molecule of negative-sense, single-
stranded RNA, 13–19 kb in size
RNA does not contain a 5’ cap & is not polyadenylated at the 3’ end, but have
functional 5’ & 3’ non-coding elements
Members of Pneumovirinae, genomic size follows the “rule of six”—that is,
number of nucleotides is a multiple of six, which appears to be a function of
binding properties of N protein to RNA molecule
Around 6–10 genes separated by conserved non-coding sequences that have
termination, polyadenylation, & initiation signals for the transcribed mRNAs
Respirovirus, Avulavirus, Henipavirus, & Morbillivirus have 6 genes, genus
Rubulavirus have 7, genus Metapneumovirus has 8, & genus Pneumovirus
has 10
6. Most of the gene products are present in virions either associated with the lipid
envelope or complexed with virion RNA
Virion proteins include three nucleocapsid proteins (RNA-binding protein (N),
phosphoprotein(P), & large polymerase protein (L))
Three membrane proteins (an unglycosylated matrix protein (M), & two
glycosylated envelope proteins—a fusion protein (F) & an attachment protein, the
latter being a hemagglutinin (H), a hemagglutinin–neuraminidase (HN), or a
glycoproteinG that has neither hemagglutinating nor neuraminidase activities].
Variably conserved proteins include non-structural proteins (C, NS1, NS2), a
cysteine-rich protein (V) that binds zinc, a small integral membrane protein (SH),
& transcription factors M2-1 & M2-2
Envelope spikes of paramyxoviruses are composed of two glycoproteins: the
fusion protein (F) & HN (Respirovirus, Avulavirus, Rubulavirus), H (Morbillivirus),
or G (Henipavirus, Pneumovirus, Metapneumovirus)
7. Both envelope proteins have key roles in the pathogenesis of all
paramyxovirus infections
One glycoprotein (HN, H, or G) is responsible for cell attachment, but
other (F) mediates the fusion of viral envelope with the plasma
membrane of the host cell
Fusion protein is synthesized as an inactive precursor (F0) that must be
activated by proteolytic cleavage by cellular proteases
Cleavage of F0 is essential for infectivity, & is a key determinant of
pathogenicity
M or matrix protein is the most abundant protein in the virion
M interacts with the lipid envelope, cytoplasmic “tails” of the F- & HN-
like proteins, & ribonucleoprotein
Interactions are consistent with M having a central role in the assembly
of mature virions
11. Virus Replication
Formation of syncytia is a characteristic feature of many paramyxovirus
Acidophilic cytoplasmic inclusions composed of ribonucleoprotein structures are
characteristic of paramyxovirus infections -replication is entirely cytoplasmic
Morbilliviruses also produce characteristic acidophilic intranuclear inclusions
that are complexes of nuclear elements & N protein
Hemadsorption is a distinctive feature of paramyxoviruses that encode an HN
protein
Paramyxoviruses replicate in the cytoplasm of infected cells;
virus replication continues in the presence of actinomycin D & in enucleated
cells, confirming that there is no requirement for nuclear functions
Virus attachment proteins (HN, H, G), recognize compatible ligands on the
surface of host cells
Rubulaviruses, respiroviruses, & avulaviruses, HN binds to surface molecules
having sialic acid residues—glycolipids or glycoproteins
12. After attachment, processed F protein mediates fusion of the viral envelope by
plasma membrane at physiologic pH
Liberated nucleocapsid remain intact, by all three of related proteins (N, P, & L)
being necessary for initial transcription of the genomic viral RNA by the RNA-
dependent RNA polymerase [transcriptase (L)];
mRNA synthesis is initiated in the absence of protein synthesis
Polymerase complex initiates RNA synthesis at a single site on the 3’ end of
genomic RNA, RNA is transcribed & N protein binds to the nascent RNA chain
This alters the polymerase to ignore the message- termination signals, &
complete positive-sense antigenome strand is made
This antigenome strand complexed with N protein then serves as a template for
the production of negative-sense genomic RNA
A second phase of mRNA synthesis then begins from the newly made genomic
RNA, thus amplifying dramatically the synthesis of viral proteins
13. But most genes encode a single protein, P gene of the member viruses of the
subfamily Paramyxovirinae encodes three to seven P/V/C proteins
P gene is essential for virus replication
C-terminal of the protein binds to L protein & N protein RNA complex to form a
unit that is essential for mRNA transcription
N-terminal portion of the P protein is also proposed to bind to the newly
synthesized N protein to permit synthesis of genomic RNA from the plus-strand
template.
Protein products of the “P gene” of several paramyxoviruses, including
henipaviruses & morbilliviruses, disrupt innate host defenses
P gene compromise the interferon response network, maybe over inhibition of
the signal transducers & activator of transcription (STAT) proteins, interferon
regulatory factor 3 (IRF3), & other interferon response genes
14. Virion maturation involves:
Incorporation of viral glycoproteins into patches on the host-cell plasma
membrane;
Association of matrix protein (M) & other non-glycosylated proteins with this
altered host-cell membrane;
Alignment of nucleocapsid beneath the M protein;
Formation & release via budding of mature virions
MEMBERS OF THE SUBFAMILY PARAMYXOVIRINAE, GENUS RESPIROVIRUS
Bovine parainfluenza virus 3
It is the potential role of the virus in initiating so-called shipping fever of cattle, or
bovine respiratory disease complex, which has prompted most attention &
controversy
Shipping fever occurs in cattle following to transportation or stressful situations;
term refers to an ill-defined disease syndrome caused by a variety of agents acting
in concert or sequentially, culminating in severe bacterial bronchopneumonia that
is most commonly caused by Mannheimia haemolytica
Syndrome remains an economically important problem, particularly in feedlots
15. Clinical Features & epidemiology
Bovine parainfluenza virus 3 has a worldwide distribution & can infect
many species of ungulates, including cattle, sheep, goats, & wild
ruminants, as well as humans & non-human primates
In calves, lambs, & goat kids, infection is generally subclinical, but
sometimes may manifest as fever, lacrimation, serous nasal discharge,
depression, dyspnea, & coughing
Some animals develop bronchointerstitial pneumonia that selectively
affects anteroventral portions of the lungs
Uncomplicated respiratory infection caused by bovine parainfluenza virus
3 runs a brief clinical course of 3–4 days that usually followed- complete
& uneventful recovery
But, stressful circumstances, cattle & sheep may subsequently develop
severe bacterial bronchopneumonia—that is, shipping fever.
16. Poor hygiene, crowding, transport, harsh climatic conditions, & other
causes of stress typically initiate this important disease syndrome
Pathogenesis & Pathology
Infection results in necrosis & inflammation in small airways in the
lungs—specifically bronchiolitis & bronchitis—with accumulation of
cellular exudate in the lumen of affected airways
Epithelial cells of the respiratory tract are the primary target cells bovine
parainfluenza virus 3, but type II pneumocytes & alveolar macrophages
also infected, sometimes with the presence of acidophilic
intracytoplasmic & /or intranuclear inclusion bodies
Infection of alveolar macrophages & interference with the normal
protective mucociliary clearance mechanisms of the lung predispose to
bacterial invasion & pneumonia
17. Diagnosis
Diagnosis of bovine parainfluenza virus 3 infection is most often made by
virus isolation or serology to demonstrate increasing antibody titers.
Available serological assays include hemagglutination-inhibition & virus
neutralization
Nasal swabs or tracheal wash fluids are the samples of choice for virus
detection, & virus can be recovered from the nasal discharges for 7–9
days after infection, by cultivation in bovine cell cultures.
Virus may be identified in nasal discharges or respiratory tissues by
immunofluorescence staining,
RT-PCR tests, or
immunohistochemistry
18. Immunity, Prevention, & Control
Convalescent animals develop a strong immune response, indicated by
presence of virus-specific antibodies that mediate hemagglutination-
inhibition, neuraminidase inhibition, & virus neutralization
Antibodies are predominantly directed against the hemagglutinin–
neuraminidase protein
Sterile immunity is short lived, as it is with many respiratory pathogens, &
animals become susceptible to reinfection after several months
Colostral antibodies prevent clinical disease
Inactivated & live-attenuated virus vaccines for intranasal & parenteral
use are available that induce protective antibodies
19. MEMBERS OF THE SUBFAMILY PARAMYXOVIRINAE, GENUS AVULAVIRUS
ND & OTHER AVIAN PARAMYXOVIRUS TYPE 1 VIRUSES
ND has become one of the most important diseases of poultry worldwide,
negatively affecting trade & poultry production in both developing & developed
countries
Disease was first observed in Java, Indonesia, in 1926, & same year it spread to
England, where it was first recognized in Newcastle-upon-Tyne, hence the
name
Disease is one of most contagious of all viral diseases, spreading rapidly among
susceptible birds
Avulavirus in the avian paramyxovirus serotype 1 group, but some virus strains
in this group are not ND virus, as they are either avirulent or of low virulence.
Genus Avulavirus also contains other species of low-virulent avian
paramyxoviruses, designated as avian paramyxoviruses 2–9
20. As of the severe economic consequences of an out-break of virulent ND in
commercial poultry, disease is reportable to the World Organization for
Animal Health (Office International des Epizooties: OIE)
Disease is defined as an infection of birds caused by an avian
paramyxovirus serotype 1 virus that meets one of the following criteria for
virulence:
(1) Virus has an intracerebral pathogenicity index in day-old chickens
(Gallus gallus domesticus) of 0.7 or greater, or
(2) Multiple basic amino acids have been demonstrated in the virus (either
directly or deduced) at the C-terminus of the F2 protein & phenylalanine
at residue 117, which is the N-terminus of the F1 protein
Term “multiple basic amino acids” refers to at least three arginine or
lysine residues between residues 113 & 116
21. Clinical Features & epidemiology
Chickens, turkeys, pheasants, guinea fowl, Muscovy & domestic ducks, geese,
pigeons, and a wide range of captive & free-ranging semi-domestic & free-
living birds, with migratory waterfowl, are susceptible to avian paramyxovirus
serotype 1 infections, including virulent strains—that, Newcastle disease virus
Introduction of the ND virus into a country has been documented through the
smuggling of exotic birds & illegal trade in poultry & poultry products
Clinical signs associated with avian paramyxovirus serotype 1 viral infections in
chickens are highly variable and dependent on the virus strain, thus virus
strains have been grouped into five pathotypes: (1) viscerotropic velogenic; (2)
neurotropic velogenic; (3) mesogenic; (4) lentogenic; (5) asymptomatic enteric.
Viscerotropic, neurotropic, & mesogenic strains are those that produce
moderate to high mortality rates & are associated with officially designated
Newcastle disease.
22. But velogenic strains kill virtually 100% of infected fowl, naturally avirulent
strains of avian paramyxovirus serotype 1 virus (lentogenic & enteric strains)
have even been used as vaccines against ND disease because they induce
cross-protective antibodies
Transmission occurs by direct contact btw birds via inhalation aerosols & dust
particles, or via ingestion of contaminated feed & water, as respiratory
secretions & feces contain high concentrations of virus
Mechanical spread between flocks is facilitated by the relative stability of the
virus & its wide host range
ND virus & excrete virus intermittently for more than 1 year without showing
clinical signs
Virus may also be disseminated by frozen chickens, uncooked kitchen refuse,
foodstuffs, bedding, manure, & transport containers.
Greatest risk for spread is via human activity, through mechanical transfer of
infective material on equipment, supplies, clothing, shoes, & other fomites.
Wind-borne transmission & movement by wild birds are much less common
modes of transfer
23. Respiratory, circulatory, gastrointestinal, & nervous signs are all
characteristic of avian paramyxovirus serotype 1 viral infections in
chickens;
Particular set of clinical manifestations depends on the age & immune
status of the host & on the virulence & tropism of infecting virus strain.
Incubation period ranges 2 to 15 days, with an average of 5–6 days
Velogenic strains may cause high mortality— close to 100%—without
clinical signs
Some birds will have neurological signs with muscle tremors, torticollis,
paralysis of legs & wings, & opisthotonos
Neurotropic strains produce severe respiratory disease followed, in 1–2
days, by neurological signs & near cessation of egg production.
Infection produces 100% morbidity, but only 50% mortality, in adult
chickens; mortality is higher in young birds
24. Mesogenic strains produce respiratory disease, reduced egg production &,
uncommonly, neurological signs, & low mortality
Lentogenic strains usually cause no disease unless accompanied by secondary
bacterial infections that result in respiratory signs
Pathogenesis & Pathology
Strains of avian paramyxovirus serotype 1 virus differ widely in virulence,
depending on the cleavability & activation of the fusion (F) glycoprotein
Low-virulent or avirulent virus strains produce precursor F proteins that are
cleaved only by a trypsin-like protease that has a restricted tissue distribution,
& which is usually present extracellularly or in epithelial cells of only the
respiratory & digestive systems.
In contrast, in virulent virus strains these precursor F proteins are cleaved
intracellularly by furin-like proteases present in cells lining mucous
membranes
Relative ease of intracellular cleavage allows virulent viruses to replicate in
more cell types, with attendant wide-spread tissue injury, viremia & systemic
disease
25. Avian paramyxovirus serotype 1 virus initially replicates in the mucosal
epithelium of the upper respiratory & intestinal tracts, which for lentogenic &
enteric strains means that disease is limited to these two systems, with
airsacculitis being most prominent
For virulent Newcastle disease viruses the virus quickly spreads after infection
via the blood to the spleen & bone marrow, producing a secondary viremia that
leads to infection of other target organs
Gross lesions include ecchymotic hemorrhages in larynx, trachea, esophagus, &
in intestine
Prominent histologic lesions are foci of necrosis in intestinal mucosa, mainly
associated with Peyer’s patches & cecal tonsil, submucosal lymphoid tissues, &
primary & secondary lymphoid tissues, & generalized vascular congestion in
most organs, with the brain
26. Virulent velogenic strains cause marked hemorrhage, in particular at the
junctions of the esophagus & proventriculus, & proventriculus & gizzard, & in
the posterior half of the small intestine
Diagnosis
ND confirmed by virus isolation, RT-PCR, & serology.
Virus may be isolated from spleen, brain, or lungs from dead birds, or tracheal &
cloacal swabs from either dead or live birds, by allantoic sac inoculation of 9–10-
day-old embryonating eggs
Demonstration of antibody is diagnostic only in unvaccinated flocks;
hemagglutination-inhibition is the test of choice as of the rapidity of the test
results
Commercial ELISA kits provide a convenient alternative, but most ELISA tests are
only applicable for chickens & turkeys
27. Immunity, Prevention, & Control
Antibody production is rapid after infection, & hemagglutination-inhibiting &
virus-neutralizing antibody can be detected within 6–10 days of infection, peaks
at 3–4 weeks, & persists over a year
Maternal antibodies transferred via egg yolk protect chicks for 3–4 weeks after
hatching as they have a half-life of approximately 4.5 days
IgG is confined to the circulation & does not prevent respiratory infection, but it
does block viremia
Where the disease is enzootic, control can be achieved by good hygiene
combined with immunization, both live-virus vaccines containing naturally
occurring lentogenic virus strains & inactivated virus (injectable oil emulsions)
being usually used
New-generation vectored vaccines have been developed
28. MEMBERS OF THE SUBFAMILY PARAMYXOVIRINAE, GENUS MORBILLIVIRUS
Members of the genus Morbillivirus all utilize the same replication strategy & all lack
neuraminidase activity
RINDERPEST VIRUS
Rinderpest is one of the oldest recorded plagues of livestock
It most probably arose in Asia, & was described in 4th century
Causative agent, rinderpest virus, was first shown to be a filterable virus in 1902
On the basis of phylogenetic analysis, it has been suggested that rinderpest virus is the
archetype morbillivirus, speculated to have given rise to canine distemper & human measles
viruses - 5000 to 10,000 years ago
Clinical Features & epidemiology
Rinderpest is a highly contagious disease of cattle & other artiodactyls
Host range includes domestic cattle, water buffalo, yak, sheep, & goats
In its typical manifestation, rinderpest is an acute febrile disease with morbidity in susceptible
populations 100% & mortality 50% (range 25–90%)
After incubation period of 3–5 days, there is a prodromal phase with rapid increase in
temperature, decrease in milk production, labored breathing, & cessation of eating
29. Followed by congestion of mucous membranes of conjunctiva & oral & nasal cavities, & an
abundant serous or mucoid oculonasal discharge.
Severe cases are characterized by extensive, typically coalescing, erosion & ulceration of
epithelial lining of the entire oral cavity;
plaques of caseous necrotic debris overlie foci of epithelial necrosis & inflammation, &
affected animals typically drool saliva as of the discomfort associated with swallowing.
Followed by a phase of severe bloody diarrhea & prostration caused by involvement of the GIT
Finally there is a precipitous drop in temperature, at which time affected animals may die from
dehydration & shock.
Disease also is often less severe in sheep & goats
Infection is maintained in enzootic areas in younger animals that become infected as their
maternal immunity wanes.
Rinderpest virus also can be maintained for long periods over subclinical infections in wildlife,
which serve as a reservoir for infection of cattle
Virus is relatively labile in the environment, thus transmission in enzootic areas
predominantly is by direct contact btw infected & susceptible animals.
30. Aerosol transmission occur, & virus spread by fomites
Pathogenesis & Pathology
Virus entry via infected aerosols, rinderpest virus first replicates within mononuclear
leukocytes in tonsils & mandibular & pharyngeal lymph nodes.
Within 2–3 days, virus is transported during leukocyte-associated viremia to lymphoid tissues
in the body, also the epithelium lining the gastrointestinal & respiratory tracts.
Virus utilizes the equivalent of human CD150 (signaling lymphocyte activation molecule) as a
receptor, which is stable with cellular & tissue tropism of rinderpest virus, as this molecule is
present on immature thymocytes, activated lymphocytes, macrophages, & dendritic cells
Virus also infects & replicates in endothelial cells & some epithelial cells, presumably through
a CD150-independent pathway, causing multifocal necrosis & inflammation in a variety of
mucous membranes
Rinderpest virus infection triggers a rapid innate & acquired immune response, including a
vigorous interferon response.
But, a viral protein or proteins, P protein, block the interferon response through inhibition of
the phosphorylation & nuclear translocation of STAT proteins
31. Profound lymphopenia occurs in infected animals as a consequence of virus-mediated
destruction of lymphocytes in all lymphoid tissues, with gut-associated lymphoid tissue
(Peyer’s patches).
Immune cells that support replication of rinderpest virus also produce numerous potent
immunoregulatory cytokines after appropriate stimulation
These cytokines, coupled with severe virus-induced lymphopenia, probably is responsible
for profound but transient immunosuppression that very characteristically occurs in
animals infected with rinderpest virus
Profuse diarrhea that occurs in severely affected animals rapidly leads to dehydration &
fatal hypovolemic shock
Segmental vascular congestion within the mucosa of the large intestine can produce
characteristic “zebra stripes.”
Histologic lesions include widespread necrosis of lymphocytes & multifocal epithelial
necrosis; epithelial syncytia & intracytoplasmic &, less often, intranuclear eosinophilic
inclusion bodies are characteristically present in affected tissues
32. Diagnosis
In countries where rinderpest was enzootic, clinical diagnosis was usually considered
sufficient.
Rinderpest historically could be confused with other diseases causing mucosal
congestion, erosions or ulcers, such as bovine viral diarrhea, malignant catarrhal
fever, &, in the early stages, infectious bovine rhinotracheitis & FMD
These diagnostic problems have largely been resolved with the development of
specific PCR tests for all of these “look-alike” diseases
Quantitative (real-time) RT-PCR assays available for rinderpest virus that rapidly can
distinguish it from the related peste des petits ruminants virus
ELISA used to assess prevalence of rinderpest virus infection in a given region
Importation of uncooked meat & meat products from infected countries was
forbidden, and zoo animals were quarantined before being transported to such
countries.
In countries with enzootic rinderpest & where the disease had a high probability of
being introduced, attenuated virus vaccines were used
33. PESTE DES PETITS RUMINANTS VIRUS
PPR is a highly contagious, systemic disease of goats & sheep very similar to rinderpest &
caused by a related morbillivirus, PPR
PPR grouped into four distinct lineages based on the sequence of F protein
Regardless of lineage, all strains belong to a single serogroup.
Lineages 1 & 2 occur in West Africa; lineage 3 in East Africa, Middle East, & southern India;
lineage 4 extends from the Middle East to Tibet
Transmission of the virus is similar to that of rinderpest, & requires close contact with infected
animals
Case fatality rates can be as high as 85% in goats, but rarely above 10% in sheep
In goats, a febrile response occurs at 2–8 days after infection
Clinical signs include fever, anorexia, nasal & ocular discharges, necrotic stomatitis &
gingivitis, & diarrhea.
Bronchopneumonia is a frequent complication
Diagnosis of disease, aside from clinical signs, shifted from virus isolation to quantitative RT-
PCR tests
These tests can distinguish btw PPR & rinderpest viruses, which has been critical in rinderpest
eradication program
34. A live-attenuated vaccine based on a lineage 2 virus isolate (Nigeria 75/1) is the vaccine of
choice.
CANINE DISTEMPER VIRUS
Canine distemper is a highly contagious acute febrile disease of dogs - known since at least
1760.
The continued presence of canine distemper virus in heavily vaccinated dog populations in
many countries might suggest that the virus has an other reservoir, perhaps in wildlife.
Canine distemper virus has recently emerged as a significant pathogen of the large species in
family Felidae
Clinical Features & epidemiology
Host range of canine distemper virus contains all species of families Canidae (dog, dingo, fox,
coyote, jackal, wolf)
At least seven distinct lineages of canine distemper are recognized worldwide, based on
sequence analysis of the H gene: Asia-1, Asia-2, American-1, America-2, Arctic-like, European
wildlife, Europe.
Despite genetic differences amongst field strains of canine distemper virus, cross-
neutralization studies show only minor antigenic changes are not considered major enough to
warrant changes in existing vaccines
35. Dogs with mild disease exhibit fever, signs of upper respiratory tract infection, & become
listless& inappetant.
Bilateral serous ocular discharges can become mucopurulent with coughing and labored
breathing, signs that are often indistinguishable from those of “kennel cough” (acute
respiratory disease of canines)
In severe generalized distemper, infected dogs first develop a fever after an incubation
period of 3–6 days, but a second febrile response ushers in more serious phase of the
infection that coincides with systemic spread of virus & accompanying profound
leukopenia.
Signs occurring at this time include anorexia, inflammation of the upper respiratory tract
with serous or mucopurulent nasal discharge, conjunctivitis, & depression
Neurologic manifestations of distemper occur at 1–3 weeks after the onset of acute signs,
but may also appear after apparent subclinicalinfection
Seizures (so-called chewing gum fits & epileptic seizures), cerebellar & vestibular signs,
paraparesis or tetraparesis with sensory ataxia & myoclonus common
Hyperkeratosis of foot pads & nose occurs in some dogs with neurological disease, as a
result of epithelial damage caused by the virus
38. Transmission is mainly via direct contact, droplet, & aerosol, as the virus is not stable in
the environment.
Young dogs are more susceptible to the disease than older dogs, with greatest
susceptibility being between 4 & 6 months of age, after puppies lost maternal Antibody
Pathogenesis & Pathology
Canine distemper, like other morbilliviruses, infects cells express the equivalent of
human CD150 (SLAM), which present on thymocytes, activated lymphocytes,
macrophages, & dendritic cells.
Tropism of canine distemper virus for these cells explains the immunosuppressive
effects of the virus
After multiplication in regional lymph nodes, virus enters blood stream, where it
circulates within infected B & T cells.
Primary viremia is synchronous with the first bout of fever, & virus then spread to
lymphoid tissues in the body, including GALT, & fixed tissue macrophages such as Kupffer
cells in the live.
Virions formed in these sites are carried by blood mononuclear cells in secondary viremia
that coincides with second peak of fever
39. Infection of neurons & glial cells also occurs through a CD150-independent mechanism
Puppies with distemper develop pneumonia, enteritis, conjunctivitis, rhinitis, & tracheitis
Lungs are typically edematous; microscopically, there is bronchointerstitial pneumonia
with necrosis of the epithelium lining small airways, & thickening of alveolar walls.
Secondary bacterial bronchopneumonia is common as a consequence of both virus-
mediated immunosuppression & inhibition of normal pulmonary clearance mechanisms
Lesions in the CNS of infected dogs with distemper are variable, depending on duration of
infection & properties of infecting virus strain
Acidophilic inclusions may be present in the nuclei & cytoplasm of infected astrocytes,
also in epithelial cells in lung, stomach, renal pelvis, & urinary bladder
Canine distemper virus infection of neonates can result in failure of development of the
enamel of adult teeth (odontodystrophy), & metaphyseal osteosclerosisin long bones
Diagnosis
Clinical diagnosis of canine distemper can be complicated by the use of modified live
vaccines
RT-PCR is standard method of testing, but distinction of field & vaccine viruses also
requires very specialized RT-PCR assays that are not routinely available
40. Serological status of dogs can be assessed with virus neutralization assays, ELISA, or
indirect fluorescent antibody tests
Immunity, Prevention, & Control
Cell-mediated immunity is important in the protective immune response against
morbillivirus infections in general
Animals with any detectable neutralizing antibody are immune to reinfection, & immunity
after infections is life-long
Successful immunization of pups with attenuated canine distemper virus vaccines
depends on the absence of interfering maternal antibody
Age at which pups can be immunized can be predicted from a nomograph if the serum
antibody titer of the mother is known;
Instead, pups vaccinated with modified live-virus vaccine at 6 weeks of age & then at 2- to
4-week intervals until 16 weeks of age, which is the standard practice
hyper immune serum – immediately
Antibiotic therapy – secondary bacterial infection
41. MEMBERS OF THE SUBFAMILY PARAMYXOVIRINAE, GENUS HENIPAVIRUS
HENDRA VIRUS
A new virus (Hendra virus) was isolated from both affected horses & a human, & the
syndrome was reproduced experimentally in horses
Molecular analyses of the viruses isolated from horses, humans, & bats indicated a close
relationship with viruses in the genus Morbillivirus, thus the initial designation of the virus
as “equine morbillivirus.”
Clinical Features and epidemiology
Hendra virus is maintained by enzootic, asymptomatic infection in certain species of fruit
bat.
Precise mechanism of virus transmission from bats to non-natural hosts such as horses
& humans is uncertain, but through environmental contamination by secretions or
excretions from the bats (saliva, feces, urine, placental fluids).
Sporadic nature of the outbreaks is the result of changes in the feeding behavior of the
bats due to changes in food supplies or habitat incursions that facilitate close interaction
of horses & bats
42. Clinical signs include - combination of initial anorexia, depression, fever, & increased
respiratory and heart rates, followed by respiratory or neurologicalsigns
Clinical course is apparently short, with infected horses dying quickly after the onset of
clinical signs.
incubation period - 6 to 10 days
Pathogenesis and Pathology
Affected horses often exhibit severe pulmonary edema, with copious thick, foamy, &
hemorrhagic fluid in the airways.
Pericardial effusion is also characteristic
Syncytia are present in the endothelium of lung capillaries & arterioles
Cytoplasmic inclusion bodies within these syncytia
Ephrin-b2, a transmembrane protein that is expressed on endothelial cells, is the
functional receptor for the henipaviruses potentially explains distribution of virus in the
infected host
Like those of morbilliviruses, Hendra virus P gene encodes proteins that interfere with
interferon induction & signaling
This strategy of selective interference with host innate defenses very likely enhances
severity of infection.
43. Diagnosis
Epidemiology, clinical signs & florid lesions of Hendra virus infection in horses are all
distinctive, but macroscopic lesions must be distinguished - African horse sickness in
particular.
Rapid diagnosis - RT-PCR tests, & virus identified in tissues by immunofluorescence or
immunohistochemical staining
Virus isolation - done in high-containment facilities, & any work involving live virus must
be undertaken in a Bio Safety Level 4 (BSL-4) facility as of the devastating potential
consequences of human exposure.
Serological testing can be done by virus neutralization, but ELISA is much preferred as of
safety issues pertaining to the requirement to use live virus in the neutralization assay
Horses that survive Hendra virus infection develop very high titers of neutralizing
antibodies to the virus, but although vaccines are in development they are not yet
commercially available.
Hendra virus very clearly is a most dangerous zoonotic pathogen that requires
appropriate caution when its presence is suspected,
44. MEMBERS OF THE SUBFAMILY PNEUMOVIRINAE, GENUS PNEUMOVIRUS
Most pneumoviruses lack both a hemagglutinin & a neuraminidase; rather, they utilize a G
protein for cell binding
Bovine respiratory syncytial virus
bovine virus causes inapparent infections, but in recently weaned calves & young cattle it
can cause pneumonia, pulmonary edema, & emphysema
Clinical Features & epidemiology
Bovine respiratory syncytial virus infection occurs most often during the winter months
when cattle, goats, & sheep are housed in confined conditions
Protection against reinfection is short lived following natural infection, but the clinical
signs in subsequent infections are less severe.
Passive antibody is protective, in that the attack rate is less in 1-month-old calves than in
older calves with no colostral antibodies
Calves immunized with formalin-inactivated vaccine preparations developed more
severe lung injury following challenge infection with bovine respiratory syncytial virus
than did control animals, &
45. it has been proposed that the enhanced disease may be a consequence of a predominant
T-helper 2 (Th2) cell response, with the preferential release of inflammatory cytokines in
the absence of a CD8 T cell response
This abnormal Th2 cell response with eosinophilia can be reproduced by immunization
with recombinant vaccines expressing only the G protein of the virus
Several inactivated & attenuated virus vaccines are in current use
Members of the subfamily Pneumovirinae, genus Metapneumovirus
Avian rhinotracheitis virus (metapneumovirus)
Avian metapneumovirus causes a variety of disease syndromes, depending on the bird
species & virus type (types A, B, C, & D)
In young turkeys the disease is characterized by inflammation of the respiratory tract,
rales, sneezing, frothy nasal discharge, conjunctivitis, swelling of the infraorbital sinuses,
& submandibular edema.
Coughing and head shaking are frequently observed in older poults.
Exacerbated by secondary infections
Morbidity is often 100%; mortality ranges from 0.4 to 50% & highest in young poults
Swollen head syndrome is a milder form of the disease that occurs in chickens, typically
with co-infection by bacteria such as E. coli