This document summarizes key information about HIV and AIDS, including:
- HIV was discovered in 1983-1984 and is the cause of AIDS. It attacks CD4 cells in the immune system.
- HIV has structural genes (gag, pol, env) that code for viral proteins like reverse transcriptase. The virus attaches to CD4 receptors on cells via its envelope glycoproteins gp120 and gp41.
- The virus has early and late stages. Late stage HIV is T-tropic and infects T cells. This leads to declining CD4 counts and increased risk of opportunistic infections that define AIDS.
This document provides an overview of AIDS (Acquired Immunodeficiency Syndrome). It begins with an introduction defining AIDS as being caused by HIV. It then discusses the epidemiology, finding that as of 2017 approximately 36.9 million people globally are infected with HIV. It explores the etiology of AIDS, explaining that it is caused by the human immunodeficiency virus HIV. The document outlines the structure of HIV and its routes of transmission including sexual contact, intravenous drug use, and mother-to-child transmission. It describes the pathogenesis and life cycle of HIV, how it infects cells and integrates into the host cell genome. The document concludes with sections on symptoms, risk factors, diagnosis and management of AIDS.
HIV primarily infects CD4+ T-cells, establishing chronic immune activation that allows the virus to thrive. During infection, HIV uses error-prone reverse transcription to establish latent reservoirs within the host. This makes eradication of the virus difficult as it develops escape mutants to evade both humoral immunity through antibody neutralization and cellular immunity from CD8+ T cells. While monocytes, macrophages, dendritic cells and natural killer cells are less affected numerically, they show functional deficiencies that allow persistence and spread of the infection throughout the immune system.
This document provides an overview of HIV/AIDS, including its discovery in 1981, transmission routes, global prevalence, diagnosis, disease progression as CD4 counts decline, opportunistic infections, treatment with antiretrovirals, and potential side effects of treatment. It describes the virus itself and the immunological response. Key points are that transmission risk depends on viral load and type/volume of bodily fluid exposure, and treatment is generally recommended once symptomatic or if CD4 is below 200.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[3] Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.
HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[4] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[5] apoptosis of uninfected bystander cells,[6] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells.[7] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.
This document summarizes HIV and retroviruses. It discusses that retroviruses possess reverse transcriptase which converts viral RNA to DNA. HIV is classified as a lentivirus that causes AIDS. HIV was discovered in 1983 and is the causative agent of AIDS. It is a retrovirus with an RNA genome and envelope. The virus enters host cells using envelope proteins gp120 and gp41 to bind CD4 receptors. The virus has structural and regulatory genes. Infection progresses from primary infection to clinical latency to AIDS as CD4 counts decline. Opportunistic infections occur when CD4 counts drop below 200. Common infections include PCP, CMV, TB, candidiasis and cancers like Kaposi's sarcoma.
Aids – A Secondary Immunodeficiency Disordernilufarali
Secondary immunodeficiency results from exposure to agents and the most common form is AIDS caused by HIV. HIV is a lentivirus classified as HIV-1 or HIV-2. It has four stages: incubation, acute infection, latency and AIDS. Current treatment consists of combinations of at least three antiretroviral drugs from two classes. While treatment can suppress the virus and increase CD4 counts, there is no vaccine or cure for HIV/AIDS.
The document summarizes key information about HIV/AIDS, including:
- HIV is transmitted sexually, through shared needles, or mother-to-child. It causes AIDS by destroying CD4 cells.
- The disease was first recognized in 1981 in the US. The virus was isolated in 1983-1984.
- High risk groups for HIV infection include men who have sex with men, intravenous drug users, and heterosexual contact.
- HIV progresses from acute infection to asymptomatic latency to full-blown AIDS as CD4 cell counts decline below 200.
- Opportunistic infections define AIDS as the immune system is compromised.
- Diagnosis involves detecting antibodies or viral components. Treatment aims to suppress viral
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document provides an overview of AIDS (Acquired Immunodeficiency Syndrome). It begins with an introduction defining AIDS as being caused by HIV. It then discusses the epidemiology, finding that as of 2017 approximately 36.9 million people globally are infected with HIV. It explores the etiology of AIDS, explaining that it is caused by the human immunodeficiency virus HIV. The document outlines the structure of HIV and its routes of transmission including sexual contact, intravenous drug use, and mother-to-child transmission. It describes the pathogenesis and life cycle of HIV, how it infects cells and integrates into the host cell genome. The document concludes with sections on symptoms, risk factors, diagnosis and management of AIDS.
HIV primarily infects CD4+ T-cells, establishing chronic immune activation that allows the virus to thrive. During infection, HIV uses error-prone reverse transcription to establish latent reservoirs within the host. This makes eradication of the virus difficult as it develops escape mutants to evade both humoral immunity through antibody neutralization and cellular immunity from CD8+ T cells. While monocytes, macrophages, dendritic cells and natural killer cells are less affected numerically, they show functional deficiencies that allow persistence and spread of the infection throughout the immune system.
This document provides an overview of HIV/AIDS, including its discovery in 1981, transmission routes, global prevalence, diagnosis, disease progression as CD4 counts decline, opportunistic infections, treatment with antiretrovirals, and potential side effects of treatment. It describes the virus itself and the immunological response. Key points are that transmission risk depends on viral load and type/volume of bodily fluid exposure, and treatment is generally recommended once symptomatic or if CD4 is below 200.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[3] Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.
HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[4] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[5] apoptosis of uninfected bystander cells,[6] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells.[7] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.
This document summarizes HIV and retroviruses. It discusses that retroviruses possess reverse transcriptase which converts viral RNA to DNA. HIV is classified as a lentivirus that causes AIDS. HIV was discovered in 1983 and is the causative agent of AIDS. It is a retrovirus with an RNA genome and envelope. The virus enters host cells using envelope proteins gp120 and gp41 to bind CD4 receptors. The virus has structural and regulatory genes. Infection progresses from primary infection to clinical latency to AIDS as CD4 counts decline. Opportunistic infections occur when CD4 counts drop below 200. Common infections include PCP, CMV, TB, candidiasis and cancers like Kaposi's sarcoma.
Aids – A Secondary Immunodeficiency Disordernilufarali
Secondary immunodeficiency results from exposure to agents and the most common form is AIDS caused by HIV. HIV is a lentivirus classified as HIV-1 or HIV-2. It has four stages: incubation, acute infection, latency and AIDS. Current treatment consists of combinations of at least three antiretroviral drugs from two classes. While treatment can suppress the virus and increase CD4 counts, there is no vaccine or cure for HIV/AIDS.
The document summarizes key information about HIV/AIDS, including:
- HIV is transmitted sexually, through shared needles, or mother-to-child. It causes AIDS by destroying CD4 cells.
- The disease was first recognized in 1981 in the US. The virus was isolated in 1983-1984.
- High risk groups for HIV infection include men who have sex with men, intravenous drug users, and heterosexual contact.
- HIV progresses from acute infection to asymptomatic latency to full-blown AIDS as CD4 cell counts decline below 200.
- Opportunistic infections define AIDS as the immune system is compromised.
- Diagnosis involves detecting antibodies or viral components. Treatment aims to suppress viral
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document summarizes secondary immunodeficiency states and acquired immunodeficiency syndrome (AIDS). It describes AIDS as being caused by the human immunodeficiency virus (HIV) which leads to immunosuppression and opportunistic infections. The virus is transmitted through unprotected sex, blood transfusions, from mother to child, and sharing of infected needles. HIV infects immune cells like CD4+ T cells and macrophages. This results in loss of CD4+ T cells and ultimately immune system failure putting individuals at risk for infections and cancers.
This document provides information on HIV/AIDS, including:
1. HIV was discovered in 1983-1984 and is the cause of AIDS. It is a retrovirus that infects CD4 cells and progressively destroys the immune system.
2. HIV has three main genes - Gag, Env, and Pol - which code for structural proteins. The virus attaches to and enters CD4 cells via the Env protein, then uses the Pol protein to integrate its genetic material into the host cell DNA.
3. As the virus destroys CD4 cells over many years, it leaves the infected person vulnerable to opportunistic infections. AIDS is diagnosed when the CD4 count drops below 200. Common infections include PCP
This document summarizes key information about HIV/AIDS, including:
- HIV was discovered in 1983-1984 and is the cause of AIDS. It infects and destroys CD4 cells.
- HIV has three main genes - gag, pol, and env. Gag codes for core proteins, pol codes for enzymes, and env codes for envelope glycoproteins gp120 and gp41.
- HIV attaches to host cells via gp120 binding to CD4 receptors, then fuses and enters the cell. It replicates by converting RNA to DNA via reverse transcriptase.
- As CD4 cells decline due to infection, opportunistic infections can occur, eventually leading to AIDS if untreated. Common
AIDS is caused by the HIV virus, which damages immune cells called CD4+ T cells. This leaves the body vulnerable to opportunistic infections and cancers. It is transmitted via bodily fluids like blood, semen, vaginal fluid and breast milk. While treatments can slow the virus, there is currently no cure. Prevention methods focus on safe sex practices, needle safety, blood screening and education.
- AIDS is an acquired immunodeficiency caused by the HIV virus which affects T lymphocytes. It results in opportunistic infections and tumors due to a reduced helper T cell population. HIV is transmitted through sexual contact, blood exposure, and mother-to-child transmission.
- Laboratory diagnosis is by detecting antibodies through ELISA or detecting the virus directly through PCR, antigen detection, or viral culture. Treatment involves antiretroviral therapy using different classes of drugs targeting viral enzymes and entry.
Retroviruses like HIV possess the enzyme reverse transcriptase which allows the viral RNA genome to be transcribed into DNA and integrated into the host cell genome. HIV specifically infects CD4+ T cells, macrophages, and dendritic cells, hijacking their machinery to replicate. Over time, HIV destroys increasingly more of the immune system by killing infected cells, until opportunistic infections or cancers can take hold, defining the acquired immunodeficiency syndrome (AIDS) stage of the infection.
It contain all information like introduction,stages,life cycle,treatment , laboratory diagnosis and first people on earth who cured from the infection with HIV.
This document provides information on immunodeficiency and HIV/AIDS. It discusses the immune system and defines primary and secondary immunodeficiency. Primary immunodeficiency is inherited and results in defective immunity from birth. Secondary immunodeficiency is acquired through disease, malnutrition or medical treatment. The document then focuses on HIV, describing its structure, infectivity stages, diagnosis methods and vaccine targets. It outlines the three phases of HIV infection and defines AIDS as developing when CD4 counts drop below 200.
Concise discussion on essential clinical and microbiological aspects of Candia, Pneumocystis and Aspergillus infections in HIV and other immunocompromised patients.
HIV is a retrovirus with an RNA genome that causes AIDS. It has two types, HIV-1 which causes the worldwide pandemic and HIV-2 which is found mainly in West Africa. HIV-1 has many subtypes that differ in their geographic distribution. The virus has an outer membrane with glycoprotein spikes that allow it to bind to and enter host cells. It contains enzymes like reverse transcriptase and integrase that help its replication cycle of binding to host cells, integrating its genetic material into the host DNA, producing new viral proteins and particles, and ultimately destroying CD4 cells and weakening the immune system. Antiretroviral drugs target specific stages of this replication cycle to suppress the virus.
Primary immunodeficiencies are present at birth and can affect adaptive or innate immune functions. The most common secondary immunodeficiency is acquired immunodeficiency syndrome (AIDS), which is caused by the human immunodeficiency virus (HIV-1). HIV-1 infects and kills CD4+ T cells, eventually leaving the body vulnerable to opportunistic infections. While antiretroviral drugs can suppress HIV-1 and prolong life, developing an effective vaccine remains the best option to prevent the spread of AIDS.
HIV (human immunodeficiency virus) is a virus that attacks the immune system, the body's natural defense system. Without a strong immune system, the body has trouble fighting off disease. Both the virus and the infection it causes are called HIV.
Prepared By : AFC Shah Zeb Khan
Student of ICAP for CA. at RAET PAC Lahore.
Also Student of BS Botany at University of Sargodha.
Structure of Virus, modes of transmission, pathogenesis, clinical features, biochemical basis of clinical symptoms, laboratory diagnosis, treatment and prevention.
This document discusses HIV and provides several key details:
- HIV is a retrovirus that replicates via a DNA intermediate and is highly variable due to its lack of proofreading mechanisms.
- The HIV genome contains 9 genes that code for 15 proteins.
- HIV likely originated from chimpanzees in Central Africa and was first identified in the United States in the 1970s, being called GRID before being renamed AIDS.
- The document also discusses the famous "Berlin patient," Timothy Ray Brown, who was cured of HIV after receiving a stem cell transplant from a donor with a CCR5 mutation that provides resistance to HIV.
This document summarizes AIDS and HIV. It describes HIV as a retrovirus that causes AIDS by destroying CD4+ T cells and weakening the immune system. HIV infection progresses from acute infection to AIDS over many years without treatment. The virus is transmitted through bodily fluids and can be diagnosed through antibody and viral load tests. There is currently no cure for HIV/AIDS, but antiretroviral treatment can control the virus and prevent opportunistic infections associated with AIDS.
Oral Manifestation of Human Immunodeficiency VirusDr Jinki Singha
HIV infects cells of the immune system and destroys their function over time. It is classified as a retrovirus. The virus structure includes proteins like p24 and inserts its RNA into the host cell DNA using reverse transcriptase. Diagnosis is through tests detecting antibodies, antigens, or viral RNA. ELISA and Western blot are most common for antibody detection while PCR detects viral RNA. Treatment involves antiretroviral drugs during all stages to suppress the virus and prevent progression to AIDS.
- Retroviridae are a family of enveloped RNA viruses that include HIV and have been associated with cancers and AIDS. HIV is classified as a lentivirus within this family.
- There are two main theories for the origin of HIV in humans - natural transfer from chimpanzees through hunting or a contaminated oral polio vaccine.
- HIV infects CD4+ T cells using its envelope proteins to bind host receptors, then integrates into the host genome and uses host cell machinery to replicate. This evades immune detection and allows the virus to persist.
This presentation provides an overview of HIV and AIDS, including:
1. Definitions of HIV as the virus that causes AIDS and weakens the immune system, and AIDS as the final stage of HIV infection.
2. HIV-1 is the most common type worldwide and generally causes AIDS faster than HIV-2, which is mostly found in West Africa.
3. HIV is transmitted through bodily fluids and can be spread through unprotected sex, blood contact, or from mother to child during pregnancy or breastfeeding. Proper precautions can prevent transmission.
HIV was discovered in 1983-1984 as the cause of AIDS. It is a retrovirus that infects CD4+ T cells and causes AIDS by destroying the immune system. There are three main stages of HIV infection: acute infection, clinical latency, and AIDS. AIDS is diagnosed when the CD4 count drops below 200 or one of over 20 opportunistic infections or cancers develops. Antiretroviral treatment can suppress the virus and prolong the clinical latency phase.
The document summarizes key aspects of HIV and its treatment. It describes the structure of the HIV virus and the stages of early and late HIV infection. It explains how HIV attaches and replicates within cells, eventually causing AIDS through depletion of CD4 cells. Symptoms and opportunistic infections that occur are outlined. Methods of HIV transmission and testing approaches like ELISA, Western Blot, viral isolation are also summarized. Common antiretroviral drug regimens and their effects are briefly explained.
This document summarizes secondary immunodeficiency states and acquired immunodeficiency syndrome (AIDS). It describes AIDS as being caused by the human immunodeficiency virus (HIV) which leads to immunosuppression and opportunistic infections. The virus is transmitted through unprotected sex, blood transfusions, from mother to child, and sharing of infected needles. HIV infects immune cells like CD4+ T cells and macrophages. This results in loss of CD4+ T cells and ultimately immune system failure putting individuals at risk for infections and cancers.
This document provides information on HIV/AIDS, including:
1. HIV was discovered in 1983-1984 and is the cause of AIDS. It is a retrovirus that infects CD4 cells and progressively destroys the immune system.
2. HIV has three main genes - Gag, Env, and Pol - which code for structural proteins. The virus attaches to and enters CD4 cells via the Env protein, then uses the Pol protein to integrate its genetic material into the host cell DNA.
3. As the virus destroys CD4 cells over many years, it leaves the infected person vulnerable to opportunistic infections. AIDS is diagnosed when the CD4 count drops below 200. Common infections include PCP
This document summarizes key information about HIV/AIDS, including:
- HIV was discovered in 1983-1984 and is the cause of AIDS. It infects and destroys CD4 cells.
- HIV has three main genes - gag, pol, and env. Gag codes for core proteins, pol codes for enzymes, and env codes for envelope glycoproteins gp120 and gp41.
- HIV attaches to host cells via gp120 binding to CD4 receptors, then fuses and enters the cell. It replicates by converting RNA to DNA via reverse transcriptase.
- As CD4 cells decline due to infection, opportunistic infections can occur, eventually leading to AIDS if untreated. Common
AIDS is caused by the HIV virus, which damages immune cells called CD4+ T cells. This leaves the body vulnerable to opportunistic infections and cancers. It is transmitted via bodily fluids like blood, semen, vaginal fluid and breast milk. While treatments can slow the virus, there is currently no cure. Prevention methods focus on safe sex practices, needle safety, blood screening and education.
- AIDS is an acquired immunodeficiency caused by the HIV virus which affects T lymphocytes. It results in opportunistic infections and tumors due to a reduced helper T cell population. HIV is transmitted through sexual contact, blood exposure, and mother-to-child transmission.
- Laboratory diagnosis is by detecting antibodies through ELISA or detecting the virus directly through PCR, antigen detection, or viral culture. Treatment involves antiretroviral therapy using different classes of drugs targeting viral enzymes and entry.
Retroviruses like HIV possess the enzyme reverse transcriptase which allows the viral RNA genome to be transcribed into DNA and integrated into the host cell genome. HIV specifically infects CD4+ T cells, macrophages, and dendritic cells, hijacking their machinery to replicate. Over time, HIV destroys increasingly more of the immune system by killing infected cells, until opportunistic infections or cancers can take hold, defining the acquired immunodeficiency syndrome (AIDS) stage of the infection.
It contain all information like introduction,stages,life cycle,treatment , laboratory diagnosis and first people on earth who cured from the infection with HIV.
This document provides information on immunodeficiency and HIV/AIDS. It discusses the immune system and defines primary and secondary immunodeficiency. Primary immunodeficiency is inherited and results in defective immunity from birth. Secondary immunodeficiency is acquired through disease, malnutrition or medical treatment. The document then focuses on HIV, describing its structure, infectivity stages, diagnosis methods and vaccine targets. It outlines the three phases of HIV infection and defines AIDS as developing when CD4 counts drop below 200.
Concise discussion on essential clinical and microbiological aspects of Candia, Pneumocystis and Aspergillus infections in HIV and other immunocompromised patients.
HIV is a retrovirus with an RNA genome that causes AIDS. It has two types, HIV-1 which causes the worldwide pandemic and HIV-2 which is found mainly in West Africa. HIV-1 has many subtypes that differ in their geographic distribution. The virus has an outer membrane with glycoprotein spikes that allow it to bind to and enter host cells. It contains enzymes like reverse transcriptase and integrase that help its replication cycle of binding to host cells, integrating its genetic material into the host DNA, producing new viral proteins and particles, and ultimately destroying CD4 cells and weakening the immune system. Antiretroviral drugs target specific stages of this replication cycle to suppress the virus.
Primary immunodeficiencies are present at birth and can affect adaptive or innate immune functions. The most common secondary immunodeficiency is acquired immunodeficiency syndrome (AIDS), which is caused by the human immunodeficiency virus (HIV-1). HIV-1 infects and kills CD4+ T cells, eventually leaving the body vulnerable to opportunistic infections. While antiretroviral drugs can suppress HIV-1 and prolong life, developing an effective vaccine remains the best option to prevent the spread of AIDS.
HIV (human immunodeficiency virus) is a virus that attacks the immune system, the body's natural defense system. Without a strong immune system, the body has trouble fighting off disease. Both the virus and the infection it causes are called HIV.
Prepared By : AFC Shah Zeb Khan
Student of ICAP for CA. at RAET PAC Lahore.
Also Student of BS Botany at University of Sargodha.
Structure of Virus, modes of transmission, pathogenesis, clinical features, biochemical basis of clinical symptoms, laboratory diagnosis, treatment and prevention.
This document discusses HIV and provides several key details:
- HIV is a retrovirus that replicates via a DNA intermediate and is highly variable due to its lack of proofreading mechanisms.
- The HIV genome contains 9 genes that code for 15 proteins.
- HIV likely originated from chimpanzees in Central Africa and was first identified in the United States in the 1970s, being called GRID before being renamed AIDS.
- The document also discusses the famous "Berlin patient," Timothy Ray Brown, who was cured of HIV after receiving a stem cell transplant from a donor with a CCR5 mutation that provides resistance to HIV.
This document summarizes AIDS and HIV. It describes HIV as a retrovirus that causes AIDS by destroying CD4+ T cells and weakening the immune system. HIV infection progresses from acute infection to AIDS over many years without treatment. The virus is transmitted through bodily fluids and can be diagnosed through antibody and viral load tests. There is currently no cure for HIV/AIDS, but antiretroviral treatment can control the virus and prevent opportunistic infections associated with AIDS.
Oral Manifestation of Human Immunodeficiency VirusDr Jinki Singha
HIV infects cells of the immune system and destroys their function over time. It is classified as a retrovirus. The virus structure includes proteins like p24 and inserts its RNA into the host cell DNA using reverse transcriptase. Diagnosis is through tests detecting antibodies, antigens, or viral RNA. ELISA and Western blot are most common for antibody detection while PCR detects viral RNA. Treatment involves antiretroviral drugs during all stages to suppress the virus and prevent progression to AIDS.
- Retroviridae are a family of enveloped RNA viruses that include HIV and have been associated with cancers and AIDS. HIV is classified as a lentivirus within this family.
- There are two main theories for the origin of HIV in humans - natural transfer from chimpanzees through hunting or a contaminated oral polio vaccine.
- HIV infects CD4+ T cells using its envelope proteins to bind host receptors, then integrates into the host genome and uses host cell machinery to replicate. This evades immune detection and allows the virus to persist.
This presentation provides an overview of HIV and AIDS, including:
1. Definitions of HIV as the virus that causes AIDS and weakens the immune system, and AIDS as the final stage of HIV infection.
2. HIV-1 is the most common type worldwide and generally causes AIDS faster than HIV-2, which is mostly found in West Africa.
3. HIV is transmitted through bodily fluids and can be spread through unprotected sex, blood contact, or from mother to child during pregnancy or breastfeeding. Proper precautions can prevent transmission.
HIV was discovered in 1983-1984 as the cause of AIDS. It is a retrovirus that infects CD4+ T cells and causes AIDS by destroying the immune system. There are three main stages of HIV infection: acute infection, clinical latency, and AIDS. AIDS is diagnosed when the CD4 count drops below 200 or one of over 20 opportunistic infections or cancers develops. Antiretroviral treatment can suppress the virus and prolong the clinical latency phase.
The document summarizes key aspects of HIV and its treatment. It describes the structure of the HIV virus and the stages of early and late HIV infection. It explains how HIV attaches and replicates within cells, eventually causing AIDS through depletion of CD4 cells. Symptoms and opportunistic infections that occur are outlined. Methods of HIV transmission and testing approaches like ELISA, Western Blot, viral isolation are also summarized. Common antiretroviral drug regimens and their effects are briefly explained.
HIV infects and destroys CD4+ T cells, leading to immunosuppression and opportunistic infections. In 1981, the first AIDS cases were reported in homosexual men with PCP. HIV was identified as the cause in 1984. It is transmitted sexually or through blood/bodily fluids. Profound CD4+ T cell loss and impaired immune response are hallmarks of AIDS. Opportunistic infections like PCP occur when CD4+ levels drop below 200. Antiretroviral therapy and treatment/prophylaxis of opportunistic infections can improve health and longevity for those with HIV/AIDS.
The document summarizes key information about HIV/AIDS, including:
1) HIV is a lentivirus that causes AIDS by progressively destroying the immune system, allowing other infections to thrive. Once infected, the body cannot rid itself of HIV.
2) Scientists believe HIV originated from chimpanzees in West Africa and was transmitted to humans through contact with their blood.
3) HIV is classified as a retrovirus and exists as two types, HIV-1 and HIV-2. HIV-1 is more widespread and virulent.
4) There is no cure for HIV, but treatment with antiretroviral drugs can control the virus and prevent transmission.
HIV is a retrovirus that infects CD4+ T cells and causes AIDS by destroying the immune system. It enters the body through sexual contact, blood transmission, or during birth. Once inside it spreads to lymphoid tissues where it replicates within T cells and macrophages. This causes cell dysfunction and death, damaging the immune system over time. Despite an immune response, HIV evolves rapidly and establishes reservoirs that allow lifelong persistence. Without treatment, this progressive immune destruction ultimately results in AIDS.
The document discusses Acquired Immunodeficiency Syndrome (AIDS), which is caused by the human immunodeficiency virus (HIV). It is transmitted through unprotected sex, contaminated blood transfusions, hypodermic needles, and during pregnancy or breastfeeding. There is currently no cure for AIDS, but treatment involves antiretroviral therapy to suppress HIV and prevent opportunistic infections. Scientists are working to develop more effective treatments such as protease inhibitors, fusion inhibitors, and integrase inhibitors.
This document provides an overview of AIDS/HIV, including:
- HIV attacks and damages the immune system, leading to AIDS. It was first observed in 1981 in homosexual males. Currently, around 35 million people live with HIV globally.
- HIV is a retrovirus that inserts its RNA into the DNA of host cells using the enzyme reverse transcriptase. There are two main types: HIV-1 is more common and transmissible, while HIV-2 is limited to certain regions.
- HIV infects CD4+ immune cells like T-cells using its envelope proteins gp120 and gp41 to bind and fuse with the host cell membrane. It is primarily transmitted through unprotected sex, contaminated blood, and from mother
This document provides information on HIV infection in pregnancy. It discusses that HIV can be transmitted from mother to child during pregnancy, childbirth, or breastfeeding. The key strategies to prevent mother-to-child transmission include testing pregnant women for HIV, treating HIV-positive pregnant and breastfeeding women with antiretroviral therapy, safe delivery practices, and guidance on infant feeding options. With effective interventions, the risk of transmission can be reduced to less than 5%.
The document discusses AIDS (acquired immunodeficiency syndrome), which is caused by HIV (human immunodeficiency virus) infection. It defines AIDS and describes the pathophysiology, risk factors, clinical manifestations, diagnostic tests, medical management including antiretroviral drugs, and nursing management of patients with AIDS. It also summarizes a research study on the use of first-line antiretroviral therapy from an ART program clinic in Pune, India.
The document provides an overview of HIV and AIDS, including:
- The origin and history of HIV, tracing it back to transfers from chimpanzees to humans in Africa in the late 19th/early 20th century.
- The structure and life cycle of HIV, which involves adsorption, penetration, reverse transcription, integration, transcription, and assembly/release of new virus particles.
- How HIV interacts with and affects the immune system, preferentially infecting CD4+ T cells and macrophages/monocytes and ultimately causing immunosuppression.
- The four stages of HIV infection: primary infection, asymptomatic stage, symptomatic stage, and AIDS.
This document discusses acute HIV infection and CDC criteria for diagnosis. It defines acute HIV infection as occurring within approximately six months of infection. Symptoms may include fever, lymphadenopathy, sore throat, rash, and others nonspecific symptoms. Diagnosis is made by detecting HIV RNA during the window period before antibodies develop or with a positive combination antigen/antibody test and negative antibody-only test. Early diagnosis is important for individual treatment and reducing transmission.
The document provides an overview of HIV and AIDS, including:
- HIV is a virus that weakens the immune system and can lead to AIDS if untreated. There are two types, HIV-1 being more prevalent.
- It is typically transmitted sexually, through blood/needles, or mother-to-child. Diagnosis involves antibody tests like ELISA and confirmation with Western Blot.
- If left untreated, it can take 10-15 years for HIV to develop into AIDS. Antiretroviral treatment can slow disease progression. Current global statistics and highest prevalence areas are mentioned.
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1) HIV is a retrovirus that causes AIDS by infecting CD4+ T cells and macrophages. It has an outer envelope with glycoproteins gp120 and gp41, and an inner capsid core containing its RNA genome and enzymes.
2) HIV enters cells via gp120 binding to CD4 and CCR5 receptors, then replicates by transcribing its RNA into DNA. New virions bud from the cell membrane.
3) Primary HIV infection causes flu-like symptoms. Later, without treatment, opportunistic infections and cancers develop due to immune deficiency, defining AIDS.
The document provides information on HIV/AIDS, including:
- HIV is a retrovirus that infects CD4+ T cells and macrophages, progressively destroying the immune system.
- The virus enters cells using envelope glycoproteins, and its RNA is converted to DNA by reverse transcriptase. The DNA integrates into the host cell's genome.
- As the virus replicates and destroys immune cells, it can eventually cause AIDS, characterized by opportunistic infections. Current antiretroviral treatment aims to suppress viral replication and boost the immune system.
Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV). HIV is a retrovirus that infects CD4 T-lymphocytes and causes immunosuppression. The virus is transmitted via bodily fluids like blood, semen, vaginal secretions. HIV enters cells, converts its RNA to DNA then incorporates into the host cell's genome. This leads to a reduction in CD4 cells and impairment of immune function. Over time AIDS develops, characterized by opportunistic infections as the immune system is compromised.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).
The document provides an overview of HIV and AIDS, including:
- HIV is a retrovirus that infects and destroys CD4+ T cells, ultimately leading to AIDS.
- Primary HIV infection may cause acute symptoms that resolve within months. Years later, very low CD4+ counts lead to opportunistic infections defining AIDS, like Pneumocystis pneumonia.
- Common infections include Pneumocystis jiroveci, CMV, Mycobacterium tuberculosis, and fungal infections. Kaposi's sarcoma and lymphomas are associated cancers.
It Contains Pathogenesis of viral diseases like AIDS, Hepatitis, Influenza and Rabies.
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This document provides information about HIV infections and AIDS. It begins by describing HIV and AIDS, noting it was first recognized in 1981 and is caused by the HIV virus. It then discusses epidemiology, stating that as of 2000 there were an estimated 36 million people living with HIV/AIDS worldwide and 4 million in India. The document goes on to describe the normal immune system, how HIV works including its lifecycle, and the stages of HIV infection from primary infection through disease progression. It also covers transmission methods, high risk groups, viral structure, diagnosis, oral manifestations, and prevention.
HIV causes AIDS by infecting and destroying CD4+ T cells. It is transmitted sexually or through blood/bodily fluids. After entering the body, HIV binds to CD4 receptors on T cells, integrates into the host cell DNA, and uses the cell's machinery to replicate. This leads to the destruction of infected T cells and ultimately a collapse of the immune system as CD4+ T cell counts decline severely. As the immune system is compromised, opportunistic infections and cancers then develop, characterizing the onset of AIDS.
This document discusses suffixes and terminology used in medicine. It begins by listing common combining forms used to build medical terms and their meanings. It then defines several noun, adjective, and shorter suffixes and provides their meanings. Examples are given of medical terms built using combining forms and suffixes. The document also examines specific medical concepts in more depth, such as hernias, blood cells, acromegaly, splenomegaly, and laparoscopy.
The document is a chapter from a medical textbook that discusses anatomical terminology pertaining to the body as a whole. It defines the structural organization of the body from cells to tissues to organs to systems. It also describes the body cavities and identifies the major organs contained within each cavity, as well as anatomical divisions of the abdomen and back.
This document is from a textbook on medical terminology. It discusses the basic structure of medical words and how they are built from prefixes, suffixes, and combining forms. Some key points:
- Medical terms are made up of elements including roots, suffixes, prefixes, and combining vowels. Understanding these elements is important for analyzing terms.
- Common prefixes include hypo-, epi-, and cis-. Common suffixes include -itis, -algia, and -ectomy.
- Dozens of combining forms are provided, such as gastro- meaning stomach, cardi- meaning heart, and aden- meaning gland.
- Rules are provided for analyzing terms, such as reading from the suffix backward and dropping combining vowels before suffixes starting with vowels
This document is the copyright information for Chapter 25 on Cancer from the 6th edition of the textbook Molecular Cell Biology published in 2008 by W. H. Freeman and Company. The chapter was authored by a team that includes Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
This document is the copyright information for Chapter 24 on Immunology from the 6th edition of the textbook Molecular Cell Biology published in 2008 by W. H. Freeman and Company. The chapter was authored by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
Nerve cells, also known as neurons, are highly specialized cells that process and transmit information through electrical and chemical signals. This chapter discusses the structure and function of neurons, how they communicate with each other via synapses, and how signals are propagated along neurons through changes in their membrane potentials. Neurons play a vital role in the nervous system by allowing organisms to process information and coordinate their responses.
This document is the copyright information for Chapter 22 from the 6th edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "The Molecular Cell Biology of Development" and is authored by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
This document is the copyright information for Chapter 21 from the sixth edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Cell Birth, Lineage, and Death" and is authored by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
This document is the copyright page for Chapter 20 from the 6th edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Regulating the Eukaryotic Cell Cycle" and is authored by a group of scientists including Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
This document is the copyright information for Chapter 19 from the 6th edition textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Integrating Cells into Tissues" and is authored by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
This chapter discusses microtubules and intermediate filaments, which are types of cytoskeletal filaments that help organize and move cellular components. Microtubules are involved in processes like cell division and intracellular transport, while intermediate filaments provide mechanical strength and help integrate the nucleus with the cytoplasm. Together, these filaments play important structural and functional roles in eukaryotic cells.
This chapter discusses microfilaments, which are one of the three main types of cytoskeletal filaments found in eukaryotic cells. Microfilaments are composed of actin filaments and play important roles in cell motility, structure, and intracellular transport. They allow cells to change shape and to move by contracting or extending parts of the cell surface.
This document is the copyright page for Chapter 16 from the 6th edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Signaling Pathways that Control Gene Activity" and is authored by a group of scientists including Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh and Matsudaira.
This document is the copyright page for Chapter 15 of the 6th edition textbook "Molecular Cell Biology" by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira. It provides the chapter title "Cell Signaling I: Signal Transduction and Short-Term Cellular Responses" and notes the copyright is held by W. H. Freeman and Company in 2008.
This document is the copyright page for Chapter 14 from the 6th edition textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Vesicular Traffic, Secretion, and Endocytosis" and is authored by a group of scientists including Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh and Matsudaira.
This chapter discusses how proteins are transported into membranes and organelles within cells. Proteins destined for membranes or organelles have targeting signals that are recognized by transport systems. The transport systems then direct the proteins to their proper destinations, such as inserting membrane proteins into membranes or delivering soluble proteins into organelles.
This document is the copyright information for Chapter 12 from the sixth edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Cellular Energetics" and is authored by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
This chapter discusses the transmembrane transport of ions and small molecules across cell membranes. It covers topics such as passive transport through membrane channels and pumps, as well as active transport using ATP. The chapter is from the 6th edition of the textbook Molecular Cell Biology and is copyrighted by W. H. Freeman and Company in 2008.
This document is the copyright information for Chapter 10, titled "Biomembrane Structure", from the sixth edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter was written by a team of authors including Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh and Matsudaira.
This document is the copyright information for Chapter 9 from the 6th edition of the textbook "Molecular Cell Biology" published in 2008 by W. H. Freeman and Company. The chapter is titled "Visualizing, Fractionating, and Culturing Cells" and is authored by Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira.
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
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তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
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Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
2. Introduction
• Etiologic agent of Acquired
Immunodeficiency Syndrome (AIDS).
• Discovered independently by Luc
Montagnier of France and Robert Gallo of
the US in 1983-84.
• Former names of the virus include:
– Human T cell lymphotrophic virus (HTLV-III)
– Lymphadenopathy associated virus (LAV)
– AIDS associated retrovirus (ARV)
3. Introduction
• HIV-2 discovered in 1986, antigenically
distinct virus endemic in West Africa.
• One million people infected in US, 30
million worldwide are infected.
• Leading cause of death of men aged 25-
44 and 4th leading cause of death of
women in this age group in the US.
• http://www.cnn.com/2005/HEALTH/conditions/11/17/blacks.hiv.ap/
4. Characteristics of the virus
• Icosahedral (20 sided), enveloped virus of the
lentivirus subfamily of retroviruses.
• Retroviruses transcribe RNA to DNA.
• Two viral strands of RNA found in core
surrounded by protein outer coat.
– Outer envelope contains a lipid matrix within which
specific viral glycoproteins are imbedded.
– These knob-like structures responsible for binding to
target cell.
6. HIV
• The outer shell of the virus is
known as the Viral enevlope.
Embedded in the viral
envelope is a complex protein
known as env which consists
of an outer protruding cap
glycoprotein (gp) 120, and a
stem gp14. Within the viral
envelope is an HIV protein
called p17(matrix), and within
this is the viral core or capsid,
which is made of another viral
protein p24(core antigen).
7. Structural Genes
• Three main structural genes:
– Group Specific Antigen (Gag)
– Envelope (Env)
– Polymerase (Pol)
8. Group Specific Antigen (Gag)
• Located in nucelocapsid of virus.
• Icosahedryl capsid surrounds the internal
nucleic acids made up of p24 andp15.
• p17 lies between protein core and
envelope and is embedded in the internal
portion of the envelope.
• Two additional p55 products, p7 and p9,
are nucleic acid binding proteins closely
associated with the RNA.
9. Envelope (Env)
• Envelope (Env) gene codes for envelope
proteins gp160, gp120 and gp41.
– These polyproteins will eventually be cleaved by
proteases to become HIV envelope glycoproteins
gp120 and gp41.
– gp160 cleaved to form gp120 and gp41.
– gp120 forms the 72 knobs which protrude from outer
envelope.
– gp41 is a transmembrane glycoprotein antigen that
spans the inner and outer membranes and attaches
to gp120.
– gp120 and gp41 both involved with fusion and
attachment of HIV to CD4 antigen on host cells.
10. Polymerase (Pol)
• Polymerase (Pol) codes for p66 and p51
subunits of reverse transcriptase and p31
an endonuclease.
– Located in the core, close to nucleic acids.
– Responsible for conversion of viral RNA into
DNA, integration of DNA into host cell DNA
and cleavage of protein precursors.
11. Viral Replication
• First step, HIV attaches to susceptible host cell.
– Site of attachment is the CD4 antigen found on a
variety of cells
• helper T cells
• macrophages
• monocytes
• B cells
• microglial brain cells
• intestinal cells
– T cells infected later on.
12. Early Phase HIV Infection
• In early phase HIV
infection, initial
viruses are M-tropic.
Their envelope
glycoprotein gp120 is
able to bind to CD4
molecules and
chemokine receptors
called CCR5 found on
macrophages
14. Viral Replication
• The gp120 protein on virus binds
specifically to CD4 receptor on host cell
with high affinity.
• Gp41 causes fusion of the virus to the cell
membrane.
– After fusion virus particle enters cell.
– Viral genome exposed by uncoating particle.
15. Viral Replication
• Reverse transcriptase produces viral DNA
from RNA.
– Becomes a provirus which integrates into host
DNA.
– Period of latency occurs.
• http://www.cat.cc.md.us/courses/bio141/lecguide/unit2/viruses/hivdsdna.html
16. Viral Replication
• After a period of latency lasting up to 10 years
viral replication is triggered and occurs at high
rate.
• CD4 cell may be destroyed in the process, body
attempts to replace lost CD4 cells, but over the
course of many years body is unable to keep the
count at a safe level.
• Destruction of large numbers of CD4 cause
symptoms of HIV to appear with increased
susceptibility to opportunistic infections, disease
and malignancy.
19. Viral Replication
• Methods of transmission:
– Sexual transmission, presence of STD increases
likelihood of transmission.
– Exposure to infected blood or blood products.
– Use of contaminated clotting factors by hemophiliacs.
– Sharing contaminated needles (IV drug users).
– Transplantation of infected tissues or organs.
– Mother to fetus, perinatal transmission variable,
dependent on viral load and mother’s CD 4 count.
21. Primary HIV Syndrome
• Mononucleosis-like, cold or flu-like symptoms
may occur 6 to 12 weeks after infection.
– lymphadenopathy
– fever
– rash
– headache
– Fatigue
– diarrhea
– sore throat
– neurologic manifestations.
– no symptoms may be present
22. Primary HIV Syndrome
• Symptoms are relatively nonspecific.
• HIV antibody test often negative but becomes
positive within 3 to 6 months, this process is
known as seroconversion.
• Large amount of HIV in the peripheral blood.
• Primary HIV can be diagnosed using viral load
titer assay or other tests.
• Primary HIV syndrome resolves itself and HIV
infected person remains asymptomatic for a
prolonged period of time, often years.
23. Clinical Latency Period
• HIV continues to reproduce, CD4 count
gradually declines from its normal value of 500-
1200.
• Once CD4 count drops below 500, HIV infected
person at risk for opportunistic infections.
• The following diseases are predictive of the
progression to AIDS:
– persistent herpes-zoster infection (shingles)
– oral candidiasis (thrush)
– oral hairy leukoplakia
– Kaposi’s sarcoma (KS)
25. Oral Hairy Leukoplakia
• Being that HIV reduces immunologic activity, the
intraoral environment is a prime target for chronic
secondary infections and inflammatory processes,
including OHL, which is due to the Epstein-Barr virus
under immunosuppressed conditions
26. Kaposi’s sarcoma (KS)
• Kaposi’s sarcoma
(shown) is a rare cancer
of the blood vessels that
is associated with HIV. It
manifests as bluish-red
oval-shaped patches that
may eventually become
thickened. Lesions may
appear singly or in
clusters.
27. AIDS
• CD4 count drops below 200 person is considered to
have advanced HIV disease
• If preventative medications not started the HIV infected
person is now at risk for:
– Pneumocystis carinii pneumonia (PCP)
– cryptococcal meningitis
– toxoplasmosis
• If CD4 count drops below 50:
– Mycobacterium avium
– Cytomegalovirus infections
– lymphoma
– dementia
– Most deaths occur with CD4 counts below 50.
29. Infants with HIV
• Failure to thrive
• Persistent oral candidiasis
• Hepatosplenomegaly
• Lymphadenopathy
• Recurrent diarrhea
• Recurrent bacterial infections
• Abnormal neurologic findings.
30. Immunologic Manifestations
• Early stage slight depression of CD4
count, few symptoms, temporary.
• Window of up to 6 weeks before antibody
is detected, by 6 months 95% positive.
• During window p24 antigen present, acute
viremia and antigenemia.
31. Immunologic Manifestations
• Antibodies produced to all major antigens.
– First antibodies detected produced against
gag proteins p24 and p55.
– Followed by antibody to p51, p120 and gp41
– As disease progresses antibody levels
decrease.
32. Immunologic Manifestations
• Immune abnormalities associated with increased
viral replication.
– Decrease in CD4 cells due to virus budding from
cells, fusion of uninfected cells with virally infected
cells and apoptosis.
– B cells have decreased response to antigens possibly
due to blockage of T cell/B cell interaction by binding
of viral proteins to CD4 site.
– CD8 cells initially increase and may remain elevated.
– As HIV infection progresses, CD4 T cells drop
resulting in immunosuppression and susceptibility of
patient to opportunistic infections.
– Death comes due to immuno-incompetence.
33. Immunologic Manifestations
• Immune abnormalities associated with increased
viral replication.
– Decrease in CD4 cells due to virus budding from
cells, fusion of uninfected cells with virally infected
cells and apoptosis.
– B cells have decreased response to antigens possibly
due to blockage of T cell/B cell interaction by binding
of viral proteins to CD4 site.
– CD8 cells initially increase and may remain elevated.
– As HIV infection progresses, CD4 T cells drop
resulting in immunosuppression and susceptibility of
patient to opportunistic infections.
– Death comes due to immuno-incompetence.
35. Sustiva + Truvada Treatment
• Sustiva + Truvada (FTC + tenofovor) is one of the most
popular and effective starting HIV regimens.
• Many patients will have dream/sleep/central nervous
system effects particularly in the first month (due to the
Sustiva).
• Upset stomach/bloating/gas/loose stools is also fairly
common during the first month and for most patients is
fairly mild.
• HIV levels in the blood will often drop by > 99% in the
first month and the CD4 count (marker of immune
system function) will often increase providing protection
against AIDS related diseases within weeks/months of
starting the medication.
36. Truvada
• Truvada is made up of HIV drugs from a
class called nucleoside/nucleotide reverse
transcriptase inhibitors (NRTIs), also
known as “nukes.”
• The NRTIs block reverse transcriptase, a
protein that HIV needs to make more
copies of itself. This may slow down HIV
disease
37. ‘typical’ primary HIV-1 infection
symptoms
HIV-1 p24 antigen
0 1 2 3 4 5 6 / 2 4 6 8 10
weeks years
HIV antibodies
Time following infection
HIV viral load
HIV proviral DNA
symptoms
‘window’
period
1° infection
38. Laboratory Diagnosis of HIV Infection
• Methods utilized to detect:
– Antibody
– Antigen
– Viral nucleic acid
– Virus in culture
39. ELISA Testing
• First serological test developed to detect
HIV infection.
– Easy to perform.
– Easily adapted to batch testing.
– Highly sensitive and specific.
• Antibodies detected in ELISA include
those directed against: p24, gp120, gp160
and gp41, detected first in infection and
appear in most individuals
40. ELISA Testing
• ELISA tests useful for:
– Screening blood products.
– Diagnosing and monitoring patients.
– Determining prevalence of infection.
– Research investigations.
41. ELISA Testing
• Different types of ELISA techniques used:
– indirect
– competitive
– sandwich
• ELISAs are for screening only, false
positives do occur and may be due to AI
disease, alcoholism, syphilis, and
immunoproliferative diseases.
43. Other Screening Tests
• Agglutination tests using latex particles, gelatin
particles or microbeads are coated with HIV
antigen and will agglutinate in the presence of
antibody.
• Dot-Blot Testing utilizes paper or nitrocellulose
impregnated with antigen, patient serum is
filtered through, and anti-antibody is added with
enzyme label, color change is positive.
– A rapid, cost-effective and may become an alternative
to standard ELISA and Western blot testing.
46. Western Blot
• Most popular confirmatory test.
– Utilizes a lysate prepared from HIV virus.
– The lysate is electrophoresed to separate out the HIV
proteins (antigens).
– The paper is cut into strips and reacted with test sera.
– After incubation and washing anti-antibody tagged
with radioisotope or enzyme is added.
– Specific bands form where antibody has reacted with
different antigens.
– Most critical reagent of test is purest quality HIV
antigen.
– The following antigens must be present: p17, p24,
p31, gp41, p51, p55, p66, gp120 and gp160.
47. Western Blot
• Antibodies to p24 and p55 appear earliest
but decrease or become undetectable.
• Antibodies to gp31, gp41, gp 120, and
gp160 appear later but are present
throughout all stages of the disease.
48. Western Blot
• Interpretation of results.
– No bands, negative.
– In order to be interpreted as positive a
minimum of 3 bands directed against the
following antigens must be present: p24, p31,
gp41 or gp120/160.
• CDC criteria require 2 bands of the
following: p24, gp41 or gp120/160.
49. DNA PCR
RNA PCR
p24 Ag
3rd gen ELISA
1st gen ELISA
Detuned ELISA
1wk 2wk 3wk 2mo 6mo 1yr 2yr 3yr +8yr
gp160
gp120
p68
p55
p53
gp41-45
p40
p34
p24
p18
p12
gp160
gp120
p68
p55
p53
gp41-45
p40
p34
p24
p18
p12
gp160
gp120
p68
p55
p53
gp41-45
p40
p34
p24
p18
p12
early recent / established advanced
Spectrum
of anti-HIV
testing
50. Western Blot
• Expensive – $ 80 - 100
• technically more difficult
• visual interpretation
• lack standardisation
– - performance
– - interpretation
– - indeterminate reactions –
resolution of ??
• ‘Gold Standard’ for
confirmation
51. Western Blot
• Indeterminate results are those samples that produce
bands but not enough to be positive, may be due to the
following:
– prior blood transfusions, even with non-HIV-1 infected blood
– prior or current infection with syphilis
– prior or current infection with malaria
– autoimmune diseases (e.g., diabetes, Grave’s disease, etc)
– infection with other human retroviruses
– second or subsequent pregnancies in women.
– run an alternate HIV confirmatory assay.
• Quality control of Western Blot is critical and requires
testing with strongly positive, weakly positive and
negative controls.
52. Indirect immunofluorescence
• Can be used to detect both virus and
antibody to it.
• Antibody detected by testing patient serum
against antigen applied to a slide,
incubated, washed and a fluorescent
antibody added.
• Virus is detected by fixing patient cells to
slide, incubating with antibody.
53.
54. Detection of p24 HIV antigen
• The p24-antigen screening assay is an EIA
performed on serum or plasma.
• P24 antigen only present for short time,
disappears when antibody to p24 appears.
• Anti-HIV-1 bound to membrane, incubated with
patient serum, second anti-HIV-1 antibody
attached to enzyme label is added (sandwich
technique), color change occurs.
• Optical density measured, standard curve
prepared to quantitate results.
55. Detection of p24 HIV antigen
• Positive confirmed by neutralizing
reaction, preincubate patient sample with
anti- HIV, retest, if p24 present immune
complexes form preventing binding to HIV
antibody on membrane when added.
• Test not recommended for routine
screening as appearance and rate of rise
are unpredictable.
• Sensitivity lower than ELISA.
56. Detection of p24 HIV antigen
• Most useful for the following:
– early infection suspected in seronegative
patient
– newborns
– CSF
– monitoring disease progress
57. Polymerase Chain Reaction (PCR)
• Looks for HIV DNA in the WBCs of a person.
• PCR amplifies tiny quantities of the HIV DNA present,
each cycle of PCR results in doubling of the DNA
sequences present.
• The DNA is detected by using radioactive or biotinylated
probes.
• Once DNA is amplified it is placed on nitrocellulose
paper and allowed to react with a radiolabeled probe, a
single stranded DNA fragment unique to HIV, which will
hybridize with the patient’s HIV DNA if present.
• Radioactivity is determined.
58. Virus isolation
• Virus isolation can be used to definitively
diagnose HIV.
• Best sample is peripheral blood, but can use
CSF, saliva, cervical secretions, semen, tears or
material from organ biopsy.
• Cell growth in culture is stimulated, amplifies
number of cells releasing virus.
• Cultures incubated one month, infection
confirmed by detecting reverse transcriptase or
p24 antigen in supernatant.
59. Viral Load Tests
• Viral load or viral burden is the quantity of
HIV-RNA that is in the blood.
• RNA is the genetic material of HIV that
contains information to make more virus.
60. Viral Load Tests
• Viral load tests measure the amount of HIV-RNA
in one milliliter of blood.
• Take 2 measurements 2-3 weeks apart to
determine baseline.
• Repeat every 3-6 months in conjunction with
CD4 counts to monitor viral load ant T-cell count.
• Repeat 4-6 weeks after starting or changing
antiretroviral therapy to determine effect on viral
load.
61. Testing of Neonates
• Difficult due to presence of maternal IgG
antibodies.
• Use tests to detect IgM or IgA antibodies,
IgM lacks sensitivity, IgA more promising.
• Measurement of p24 antigen.
• PCR testing may be helpful but still not
detecting antigen soon enough: 38 days to
6 months to be positive.