Human Papillomavirus, Measles, HIV and Hepatitis Viruses
The document summarizes several viruses including HPV, measles, HIV, and hepatitis viruses. It describes the structure, transmission, pathogenesis, diagnosis, and prevention of each virus. HPV is a common sexually transmitted infection that can cause genital warts and cancers. Measles is a highly contagious airborne virus prevented by the MMR vaccine. HIV attacks CD4 cells and leads to AIDS if untreated. The hepatitis viruses are transmitted through blood or feces and can cause acute or chronic liver disease or liver cancer. Vaccines and hygiene practices can prevent transmission of these viruses.
A detailed description of HIV covering virology, morphology, pathogenesis, clinical stages and manifestations, laboratory diagnosis, and diagnostic strategy, and therapeutic options and prevention.
A detailed description of HIV covering virology, morphology, pathogenesis, clinical stages and manifestations, laboratory diagnosis, and diagnostic strategy, and therapeutic options and prevention.
Dogs are the source of the vast majority of human rabies deaths, contributing up to 99% of all rabies transmissions to humans. ... Rabies is an infectious viral disease that is almost always fatal. It is a preventable viral disease of mammals most often transmitted through the bite of a rabid animal. The vast majority of rabies cases reported to the Centers for Disease Control and Prevention (CDC) each year occur in wild animals like raccoons, skunks, bats, and foxes.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
Dogs are the source of the vast majority of human rabies deaths, contributing up to 99% of all rabies transmissions to humans. ... Rabies is an infectious viral disease that is almost always fatal. It is a preventable viral disease of mammals most often transmitted through the bite of a rabid animal. The vast majority of rabies cases reported to the Centers for Disease Control and Prevention (CDC) each year occur in wild animals like raccoons, skunks, bats, and foxes.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).
What is HIV? How an HIV infections advances to AIDS? What is AIDS? What are the medicine to stop HIV replication? What are the diagnostic tests? What are the medical managements for AIDS? What are the categories of HIV infection? Symptoms of HIV infection? What should be the nurse care plan for an AIDS patient? How can people prevent HIV infection? All these questions are answered in this presentation.
Similar to human papilloma Virus ,measles,HIV and hepatitis viruses (20)
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. WHAT IS HPV
• HPV stands for human papillomavirus.There are lots of
different types of HPV.
• Genital HPV is a very common sexually transmitted
infection. No symptoms
• More than 100 types
– More than 60 cutaneous types
• Can lead to skin warts
– 40 mucosal types
• High risk – most common are HPV 16, 18, 31 and 45
causes 70% of cervical cancers
• Low risk- include HPV types 6, 11. causes 90% of ano-genital warts
•
3. How HPV looks like?
• Papillomaviruses are small, 52-55nm in
diameter.
• They are non-enveloped, icosahedral
particles.
• This shape is made up of 12 pentameric
and 60 hexameric capsomers
• Their carpsid is composed of two
proteins, a major (L1) and minor (L2).
4. HPV Transmission
• Direct skin-to-skin contact
– Usually, but not always sexual contact
• Infected birth canal
• Fomites (very rare)
• Reservoirs
• Infected human
• Mother to child through
Vaginal childbirth
5.
6. Pathogenesis
• Virus infection initially occurs in the actively dividing basal cells
in the stratum germinativum
• Virus induced hyperplasia- results in increased cell division
• The cells subsequently undergo denaturation and
hyperkeratiniztion aggregating into nascent papilloma
7. Diagnosis & Treatment
• Can be detected in a
clinical exam;
– History
– Visual exam
– Pap smears
– DNA testing
• Can be treated by
removing the warts;
• The virus cannot be
removed, so the warts may
grow back.
8. Vaccine
Two vaccines currently developed:
1. Gardasil – protects against HPV types 16, 18,
6 and 11.
2. Cervarix – protects against HPV types 16 and 18.
1
9. Measles
• Measles or Rubeola, is an acute viral illness. Single stranded,
negative sense enveloped RNA
• Caused by a virus in the family paramyxovirus
genus Morbillvurus
• The term Rubeola a Latin word was first used
to describe the disease in Middle Ages
• The incubation Period is approx. 10 days but varies from 7 to 18 days.
It is usually 14 days until the rash appears
10. Transmission
• Measles transmission is airborne by respiratory droplet nuclei spread
Or
• It can be transmitted by direct contact with infected nasal or throat
secretions
11. Sign & Symptoms
• Severe cough, conjunctivitis, coryza and Koplik’s spots on the
buccal mucosa. These are present for three to four days prior
to rash onset
• Generalised maculopapular rash, usually lasting three or more
days
• Fever (at least 38°C) present at the time of rash onset
12. Diagnosis
• Clinical diagnosis of measles requires a history of fever of at least
three days, with at least one of the three C's (cough, coryza,
conjunctivitis)
• Observation of Koplik's spots is also diagnostic of measles
• Alternatively, laboratory diagnosis of measles can be done with
confirmation of positive measles IgM antibodies or isolation of
measles virus RNA from respiratory specimens
13. • In patients where phlebotomy is not possible, saliva can be
collected for salivary measles-specific IgA testing
• The contact with any infected person in any way, including
semen through sex, saliva, or mucus, can cause infection
14. Prevention of Measles
• Isolation of cases from diagnosis until about 5-7 days after onset
of rash
• Disinfection of all articles soiled with secretion of nose and
throat
• Administration of measles immune globulin to susceptible
infants and children under 3 years of age
15. • Measles-mumps-rubella (MMR) vaccine at 9 to 12 months of
age and a second dose at four years of age
• The second dose is not a booster but is designed to vaccinate
the approximately 5% of children who do not seroconvert to
measles after the first dose of vaccine
16. Human Immunodeficiency Virus
• The human immunodeficiency virus is a lentivirus that causes
the acquired immunodeficiency syndrome (AIDS)
• Unlike some other viruses, the human body cannot get rid of
HIV. That means that once you have HIV, you have it for life
• Chimpanzee version of the immunodeficiency virus (called
simian immunodeficiency virus, or SIV) most likely was
transmitted to humans and mutated into HIV when humans
hunted these chimpanzees for meat and came into contact with
their infected blood
•
17. • Family: Retroviridae
• Subfamily:Orthoretrovirinae
• Genus:Lentivirus
• Species: HIV 1 / HIV2
HIV 1- Isolated in America, Europe & central Africa
HIV 2- In West Africa – Less virulent and not spread as widely and rapidly as
HIV 1
18. MORPHOLOGY
• It is roughly spherical - diameter of about 120 nm
• Composed of two copies of positive single stranded
RNA (Held together by protein P7) enclosed by a
conical capsid composed of viral protein P24
• The RNA genome consists of 9 genes - Three of these
genes: gag, pol, and env, contain information needed
to make the structural proteins for new virus particles.
19. • Inside of capsid are three enzymes required for HIV
replication: reverse transcriptase, integrase and protease
• A matrix composed of the viral protein P17 surrounds the
capsid ensuring the integrity of the virion particle
• The matrix is surrounded by phospholipids – 2 layers –
Embedded by (glycoprotein) – Spikes: 2 units – Gp41 and
Gp120
20. • HIV doesn't survive well outside the body
• May survive up to 7 days in dry blood
• Virus is inactivated under extreme changes of pH in
acidic and alkaline medium.
21. Transmission
• HIV is transmitted through blood, semen, vaginal fluid
and from infected mother to her child
Sexual contact – HIV is predominantly a sexual
transmitted disease
Contaminated needles
Organ transplacentation
Blood or blood products
22. Pathogenesis
• Receptor for virus is CD4 receptor. Therefore virus may
infect any cells having CD4 receptors on the surface
• The specific binding site to the virus is enveloped
glycoprotein (Gp120)
• Double stranded DNA integrated into genome of
infected cells causing latent infection
• From time to time lytic infection is initiated releasing
progeny virions which infect other cells.
• Long and variable incubation period of HIV infection is
because of the latency.
23. • Infected CD4 cells do not appear to release normal amount
of interleukins, interferon and other lymphokines.Therefore,
immune state of a person decreases
• Patients are unable to respond to new antigens.
• An important feature to HIV infection is the polyclonal
activation of B-lymphocytes.
• All classes of immunoglobulins are involved but level of
IgG and IgA particularly rose.
• In infants and children IgM is elevated. Hyper-γ-
globulinaemia is more of hindrance than help because it
is composed of mainly useless Ig
24. • Monocyte, macrophage function also affected. As a
result chemotaxis and antigen presentation and
intracellular killing by these cells are diminished.
• NK cells are also affected
25. SIGNS & SYMPTOMS
Pneumonia, bronchitis, pleuritis, meningitis, dementia,
enteritis decrease body mass, diarrhea, carposious
sarcoma and other tumors etc.
• HIV infection has 4 stages
I. Incubation period (2-4weeks)
II. Stages of primary manifestation (years)
III. Stage of secondary manifestation
IV. Terminal stage (AIDS)
26. Laboratory Diagnosis
• Total count of leukocyte and lymphocyte (detect leucopenia), CD4
cells must be counted and the ratio between CD4 and CD8 cells is
detected, counting of platelets and rising level of IgG and IgA
• ELISA TEST, if positive the Westren blot is usually administered to confirm the
diagnosis
• Immuno assay for HIVp24 antigen
• PCR
• In order to prove presence of HIV, antibodies are detected:
1. HIV-1: antibodies to gp41, gp120, gp160, p24
2. HIV-2: antibodies to gp36, gp105, gp140
27. • HOME HIV TEST
• You swab fluid from your upper and lower gums and using a kit to test it
• Results are available within 20m minutes
• If positive you need to see to doctor to confirm the diagnosis
• If negative it needs to be to repeated in three months to confirm the result
28. Prevention
• Determination of people of risk group
• Identification of source of infection and control
• Health education – Sex should be practised by avoiding
exchange of body fluid, using sterile needles and syringes
29. Hepatitis A Virus
• Causes infectious hepatitis, Spread by fecal oral route,
results from the consumption of contaminated water, shellfish,
or other food
• It is a picornavirus, 27-nm, naked, icosahedral capsid, A
positive-sense single-stranded RNA, One serotype
• Like other picornaviruses, but HAV is not cytolytic and is
released by exocytosis
• Clinical isolates are difficult to grow in cell culture
30. Pathogenesis
• Although interferon limits viral replication, natural killer and
cytotoxic T cells are required to eliminate infected cells.
• Antibody, complement, and antibody-dependent cellular
cytotoxicity also facilitate clearance of the virus and
induction of immunopathology
• Icterus resulting from the damage of the liver occurs when
cell-mediated immune response and antibody to the virus
can be detected.
31. Transmission
• Spread rapidly because most infected people are
contagious 10 to 14 days before symptoms occur.
• HAV is released in stool in high concentrations and is
spread via fecal oral route.
• Spread in contaminated water, in food, and in dirty hands.
• Raw or improperly treated sewage can taint the water
supply and contaminate shellfish
32. Sign & Symptoms
• Immune-mediated damage to the liver
• Intensify for 4-6 days before the icteric (jaundice) phase.
• Can last up to 2 months.
• Initial symptoms: fever, fatigue, nausea, loss of appetite,
vomiting, and abdominal pain.
33. Diagnosis
• Most important: anti-HAV IgM
• Classical liver enzymes
• Virus isolation is not performed.
• Treatment, Prevention, Control:
• Interrupt the fecal-oral spread.
• Prophylaxis: immune serum globulin: before or early in incubation period
• Vaccine: Killed vaccine, recommended for all children < 1 years.
34. Hepatitis B Virus
• Previously known to cause serum hepatitis.
• Spread parenterally by blood or needles, by
sexual contact, and perinatally.
• Incubation period of 3 months.
• Might be followed by chronic hepatitis.
• Causally associated with primary hepatocellular carcinoma
(PHC).
35. • Major member of hepadnaviruses.
• Small enveloped DNA virus with several unusual
properties.
• Specifically, the genome is small, circular partly double
stranded of 3200 bases.
36. • The virion includes a protein kinase and a polymerase with
reverse transcriptase and ribonuclease H activity, as well
as a P protein attached to the genome.
• The virion is surrounded by an icosahedral capsid formed
by the hepatitis B core antigen (HBcAg) and an envelope
containing three forms of glycoprotein hepatitis B surface
antigen (HBsAg).
• HBsAg-containing particles are released into the serum
37. Pathogenesis
• HBV can cause acute or chronic, symptomatic or
asymptomatic disease determined by person’s immune
response.
• HBV found majorly in blood, but also in semen, saliva, milk,
vaginal and menstrual secretions, and amniotic fluid.
• The virus starts replication after 3 days of acquisition,
symptoms may not be observed for 45 days or longer
because they are primarily caused by immunopathology.
38. Acute infection
• Less symptomatic or asymptomatic in children.
• Long incubation
• fever, malaise, anorexia, nausea, vomiting, abdominal
discomfort, and chills, jaundice, dark urine, pale stool.
39. Chronic infection
• 5-10% of cases
• One third of those people have chronic active hepatitis
(continues destruction and causes scarring of the liver,
cirrhosis, liver failure, or PHC).
• The other two third have chronic passive hepatitis
40. Lab. Diagnosis
• The initial diagnosis can be made on basis of the clinical
symptoms and the presence of liver enzymes in blood.
• Serology describes the course and the nature of the
disease
• IgM anti-HBc is the best way to diagnose a recent acute
infection.
• The amount of virus is determined by quantitative genome
assays using PCR
41. Prevention
• Hepatitis B immune globulin may be administered within a
week of exposure.
• Chronic infection treatment: drugs targeted at the polymerase
or the nucleosides analogs for a year.
• Prevention: screening blood, safe sex, avoiding some lifestyles,
wearing gloves in hospitals....
• Vaccination: recommended for infants, children, and high risk
groups of people, a series of three injections
42. Hepatitis C Structure and Pathogenesis
• The only member of the Hepacivirus genus of the Falviviridae family.
• 6 genotypes. Positive sense RNA enveloped
• Viral RNA dependent RNA polymerase (gives antigen variability).
• The ability of HCV to remain cell associated and prevent host cell
death promotes persistent infection but results in liver disease later in
life
• It’s suggested that HCV may predispose the development of PHC.
43. Transmission and signs & symptoms
• HCV is transmitted primarily in the infected blood and sexually
• Almost every HIV infected people are HCV infected too
• The high incidence of chronic asymptomatic infections promotes the
spread.
• Acute Hepatitis ends with recovery.
• Severe rapid progression to cirrhosis.
• Chronic persistence often progresses to chronic active hepatitis.
44. Diagnosis and Prevention
• Laboratory diagnosis: based on ELISA recognition of anti-HCV
antibody or detection of the RNA genome
• Genome detection and quantitation by RT-PCR, branched-chain
DNA, and related techniques.
• Precautions for preventing HCV are similar for HBV
45. Hepatitis G Virus
• Resembles HCV in many ways.
• Flavivirus. Transmitted in blood, and has a predilection for
chronic hepatitis infection.
• It is identified by detection of the genome by RT-PCR or
other methods RNA detection
46. Hepatitis D Virus
• Single-stranded RNA, circular, forms a rod shape as a
result of its extensive base pairing.
• Uses HBV and targeted cell to replicate and produce its
protein.
• HBsAg is essential for packaging the virus.
• 40% of fulminant hepatitis infections
47. Hepatitis E Virus
• Spreads by fecal oral route. Especially in contaminated water.
• Calicivirus, RNA genome, naked capsid.
• More problematic in developing countries.
• Symptoms are similar to HAV , causes only acute disease.
• Infection is serious in pregnant women (mortality of 20%).
48. References
A REVIEW ON: HIV/AIDS by Kapila, A. et al, 2016
Hepatitis: A Review on Current and Future scenario by Pallavi k, et al. 2016
California Association for Medical Lab. Technology by Les Revier
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