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.
The Paramyxoviridae is a family of single-stranded RNA viruses known to cause different types of infections in vertebrates. Examples of these infections in humans include the measles virus, mumps virus, parainfluenza virus, and respiratory syncytial virus (RSV).
Largest viruses that infect vertebrates
Can be seen under light microscope
Poxvirus diseases are characterized by skin lesions – localized or generalized
Important diseases caused by poxviruses are-
Smallpox
Monkeypox
Cowpox
Tanapox
Molluscum contagiosum
The Paramyxoviridae is a family of single-stranded RNA viruses known to cause different types of infections in vertebrates. Examples of these infections in humans include the measles virus, mumps virus, parainfluenza virus, and respiratory syncytial virus (RSV).
Largest viruses that infect vertebrates
Can be seen under light microscope
Poxvirus diseases are characterized by skin lesions – localized or generalized
Important diseases caused by poxviruses are-
Smallpox
Monkeypox
Cowpox
Tanapox
Molluscum contagiosum
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.
The rhinovirus (from the Greek ῥίς rhis "nose", gen ῥινός rhinos "of the nose", and the Latin vīrus) is the most common viral infectious agent in humans and is the predominant cause of the common cold. Rhinovirus infection proliferates in temperatures of 33–35 °C (91–95 °F), the temperatures found in the nose. Rhinoviruses belong to the genus Enterovirus in the family Picornaviridae.
The three species of rhinovirus (A, B, and C) include around 160 recognized types of human rhinovirus that differ according to their surface proteins (serotypes).[1] They are lytic in nature and are among the smallest viruses, with diameters of about 30 nanometers. By comparison, other viruses, such as smallpox and vaccinia, are around ten times larger at about 300 nanometers; while flu viruses are around 80–120 nm.
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.
The rhinovirus (from the Greek ῥίς rhis "nose", gen ῥινός rhinos "of the nose", and the Latin vīrus) is the most common viral infectious agent in humans and is the predominant cause of the common cold. Rhinovirus infection proliferates in temperatures of 33–35 °C (91–95 °F), the temperatures found in the nose. Rhinoviruses belong to the genus Enterovirus in the family Picornaviridae.
The three species of rhinovirus (A, B, and C) include around 160 recognized types of human rhinovirus that differ according to their surface proteins (serotypes).[1] They are lytic in nature and are among the smallest viruses, with diameters of about 30 nanometers. By comparison, other viruses, such as smallpox and vaccinia, are around ten times larger at about 300 nanometers; while flu viruses are around 80–120 nm.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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It contain all information like introduction,stages,life cycle,treatment , laboratory diagnosis and first people on earth who cured from the infection with HIV.
A LECTURE ON AIDS FOR FIRST MBBS STUDENTS, DEPT OF BIOCHEMISTRY.
A CLASS ON EPIDEMIOLOGY, VIROLOGY,HIV-MORPHOLOGY, GENOME, LIFE CYCLE,MODE OF TRANSMISSION, IMMUNOLOGY, PATHOPHYSIOLOGY AND PATHOGENESIS, LABORATORY DIAGNOSIS AND MANAGEMENT.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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.
2. Introduction
• Are RNA viruses that belong to family Retroviridae.
• Possess reverse transcriptase (RNA directed DNA
polymerase) enzyme which prepares a DNA copy of the
RNA genome in host cell.
3. Classification
Subfamily Genus Virus Disease
Orthoretrovirinae Retrovirus Human T-cell Lymphotropic Virus
1 (HTLV-1)- oncogenic
Adult T-cell
leukaemia/lymphoma
Virus HTLV-2 Not associated with any
disease but prevalent in
intravenous drug users
Lentivirus Human Immunodeficiency Virus
type 1 (HIV-1)
AIDS
HIV-2 AIDS
Spumaretrovirinae Spumavirus Foamy virus Found in primary cell
culture but not
associated with disease
5. Introduction
• Etiologic agent of Acquired Immunodeficiency Syndrome (AIDS).
• AIDS was 1st recognised in USA in 1981 amonst homosexuals and
drug addicts in whom incidence of Kaposi’s sarcoma & P. carinii pneumonia was
high
• Discovered independently by Luc Montagnier of France and
Robert Gallo of the US in 1983.
• Former names of the virus include:
– Lymphadenopathy associated virus (LAV) (Luc Montagnier)
– Human T cell lymphotrophic virus (HTLV-III) (Robert Gallo)
– AIDS associated retrovirus (ARV)
• 1986, HIV name was given by International Committee on Virus nomenclature.
6. Introduction
• HIV-2 discovered in 1986, antigenically distinct virus endemic in West
Africa.
• 30 million worldwide are infected. 2 million deaths every year & 2.5 million
new cases every year.
• Leading cause of death of men aged 25-44 and 4th leading cause of death
of women in this age group.
• HIV-1 in humans was believed to be acquired from chimpanzee (Pan
troglodytes troglodytes) by cross species infections (simian
immunodeficiency virus or SIVcpz).
• HIV-2 through sooty mangabeys.
7. 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.
8. Morphology
• 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 gp 41.
• 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).
10. Group Specific Antigen (Gag)
• It encodes for core and shell proteins.
• Expressed as a precursor protein, p55.
• Cleaved into p15, p17 and p24.
• p 24 can be detected in serum during early
stages of infection till the appearance of antibodies.
• The decline of anti-p24 antibody from circulation indicates
progression of illness and is an indication of antiviral
treatment
11. Envelope (Env)
• Envelope (Env) gene codes for envelope protein
gp160; 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 gp 41 both involved with fusion
and attachment of HIV to CD4 antigen on host
cells.
12. Polymerase (Pol)
• Polymerase (Pol) codes for viral enzymes
such as reverse transcriptase.
• Expressed as precursor protein p100.
• Cleaved into p 31, p 51 and p 64.
• 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.
13. Gene Products of HIV (HIV Antigens)
Gene Coding of HIV antigens Antigens
gag Core antigens p24 (Principal core antigens), p 15, p 55
Shell antigen p 18 (nucleocapsid protein)
env Envelope antigen gp 120, (principal envelope spike antigen)
gp 41 (transmembrane antigen)
pol Reverse transcriptase antigen p 31, p 51, p 64
14. Resistance
• Temperature: Inactivated at 56oC in 30 minutes and in seconds at 100oC.
• Disinfection:
– 35% Isopropyl alcohol: inactivation in 10 minutes.
– 70% ethanol
– 0.5% lysol
– 2% freshly prepared glutaraldehyde
– 0.5% sodium hypochlrite
– 3% hydrogen peroxide
• Extremes of pH (pH 1.0, pH 13.0)
• Resistant to Lyophilisation
15. Modes of transmission
• Sexual transmission, presence of STD increases
likelihood of transmission.
• Blood transfusion.
• Parenteral transmission.
• Exposure to infected blood or blood
products.
• Transplantation of infected tissues
or organs.
• Mother to fetus, perinatal transmission variable.
16.
17. Types of Exposure and Relative Risk
S.N. Types of Exposure Relative risk per
exposure (%)
1. Sexual intercourse: anal, vaginal, oral 0.1-1.0
2. Transfusion of blood and blood
products
>90
3. Tissue and organ donations 50-90
4. Injection and injuries 0.5-1.0
5. Mother to baby 30
18. Pathogenesis
Provirus is integrated into genome of the infected cell latent infection
In the cell, RNA is transcribed by reverse transcriptase into DNA (provirus)
After entry into blood stream, HIV comes into contact with CD4 lymphocyte
19. • a
HIV can be isolated from blood, lymphocytes, cell-free plasma, cervical
secretion, semen, saliva, urine, tears and breast milk.
From time to time, lytic infection is initiated and releases progeny
virions to infect other cells
Long and variable IP is due to latency
20. • a
Which leads to a marked damping effect on CMI
Viral infection can suppress the function of infected cells without
causing any structural damage
Infection causes damage to the T4 lymphocyte, T4 cells depleted in
numbers and the T4:T8 ratio is reversed.
21. • a
Dementia and other degenerative neurological lesions may also be seen
in AIDS
This renders the patient susceptible to life threatening opportunistic
infections and malignancies
Clinical manifestations in HIV infections are mainly due to failure of
immune responses.
22. Clinical Features: According to CDC, clinical course of
HIV infection
• Group I- Acute HIV infection: Acute onset of fever, malaise, sore
throat, myalgia, arthralgia, skin rash and lymphadenopathy. Viral nucleic acid or
viral p24 antigen may be detected. Antibodies to HIV usually negative. (3 to 6
months)
• Group II- Asymptomatic infection: Show positive HIV antibody tests
and are infectious. Person usually well.
23. Clinical Features: According to CDC, clinical course of
HIV infection
• Group III- Persistent generalised lymphadenopathy:
Enlarged nodes at two or more extragenital sites for at least 3 months.
• Group IV- Symptomatic HIV infection: CD4 T lymphocyte count
falls below 400 per cu. mm. Symptoms like diarrhea, fever, weight loss,
night sweats and opportunistic infection develops. Some patients develops
AIDS related complex or conditions.
24. Primary HIV Syndrome
• Cold or flu-like symptoms may occur 6 to 12 weeks after infection.
• Symptoms are relatively nonspecific.
• HIV antibody test often negative but becomes positive within 3 to 6 months
(window period), this process is known as seroconversion.
• Large amount of HIV in the peripheral blood.
• Primary HIV syndrome resolves itself and HIV infected person remains
asymptomatic for a prolonged period of time, often years (Clinical Latency).
25. 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
– Oral candidiasis (thrush)
– Oral hairy leukoplakia (Epstein Barr virus)
– Kaposi’s sarcoma 24 (KS) (Herpes Virus)
Candidiasis
Oral Hairy Leukoplakia
26. Oral Hairy Leukoplakia (OHL)
• 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 .
Kaposi’s sarcoma (KS)
• Kaposi’s sarcoma is a rare cancer of the blood vessels
that is associated with HIV caused due to Herpes virus. It
manifests as bluish-red oval-shaped patches that may
eventually become thickened. Lesions may appear singly
or in clusters.
OHL
Kaposi’s sarcoma
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 tuberculosis
– Cytomegalovirus
– Lymphoma
– Dementia
– Most deaths occur with CD4 counts below 50.
28. • When CD4+ cells fall below 200per mm3, the titre of virus
increases markedly and there is irreversible breakdown of
immune defence mechanisms, it is defined as AIDS.
• AIDS is the end stage of HIV infection.
• Most of patients with HIV die due to oppurtunistic
infections as given below :
29. Opportunistic infections and Malignancies commonly
associated with HIV infection
• Bacterial
– Mycobacterial Infection (TB
& NTB)
– M. avium complex
– Salmonellosis
• Viral
– CMV
– Herpes simplex
– Varicella-zoster
– Epstein-Bar (EB) virus
– Human herpes virus 6 (HHV6)
– Human herpes virus 8 (HHV8)
30. Opportunistic infections and Malignancies commonly
associated with HIV infection
• Mycotic
– Pnemocystis jiroveci penumonia
– Candidiasis
– Cryptococcosis
– Aspergillosis
– Histoplasmosis
– Coccidioidomycosis
31. Opportunistic infections and Malignancies commonly
associated with HIV infection
• Parasitic
– Toxoplasmosis
– Cryptosporidiosis
– Isosporiasis
– Generalised strongyloidiasis
• Malignancies
– Kaposi’s sarcoma
– B-cell lymphoma or non-Hodgkin’s
lymphoma
32. ‘Typical’ HIV-1 infection
symptoms
2 5 6 / 2 4 6 8 103 4
weeks years
Time following infection
HIV viral load
HIV- 1 p24 antigen
HIV proviral DNA
HIV antibodies
symptoms
‘window’
period
0 1
1° infection
34. Laboratory Diagnosis of HIV Infection
• Specific test for HIV
infections
– Antigen detection: p24 antigen
– Virus isolation
– Detection of viral nucleic acid
– Antibody detection
• Non-specific Tests
– Total and differential leucocyte
count
– T-lymphocyte subset assays
– Platelet count
– IgG and IgA levels
– Skin tests for CMI
Test for opportunistic infections and tumour
35. Laboratory Diagnosis of HIV Infection
• Non-specific Tests
– Total and differential
leucocyte count
– T-lymphocyte subset assays
– Platelet count
– IgG and IgA levels
– Skin tests for CMI
36. Specific Tests for HIV
• Antigen Detection
– Virus Ag (p24) & reverse transcriptase (RT) detected in blood after
two weeks.
– p24 Ag earliest marker to appear in blood.
– With seroconversion, Ab appears p24 Ag disappears remains
absent during the long asymptomatic phase.
– Ap24 Agenemia reppears with the onset of clinical disease which
corresponds to loos of anti p24 Ab
– ELISA
37. Specific Tests for HIV
• Virus isolation
– Virus +nt in blood and body fluids mostly
within CD4 lymphocytes.
– Can be isolated from CD4 lymphocytes
of blood, B.M. and serum
– Patient’s lymphocytes are co-cultivated
with uninfected human lymphocytes in
the presence of IL-2.
– Same as above.
38. Specific Tests for HIV
• Detection of Viral Nucleic acid
– PCR, useful in window period
• DNA PCR peripheral lymphocytes are lysed and proviral DNA
is amplified. Highly sensitive & specific.
• RNA PCR (RT-PCR) used for diagnosis and also for
monitoring level of viraemia
RT-PCR
39. Specific Tests for HIV
• Antibody detection
– Simplest and most commonly employed technique for diagnosis.
– Several weeks to months for Abs to appear.
– IgM3-4 weeks followed by IgG Abs
– IgM Abs disappear in 8-10 weeks while IgG Abs remains
throughout life.
– With severe immunodeficiency in AIDS, some components of anti-
HIV Ab (e.g. anti-p24) may disappear.
40. Specific Tests for HIV
– HIV infected persons remain negative for Abs during
window period, when initial viral replication takes place
for about 2-3 weeks.
41. Specific Tests for Lab Diagnosis of HIV Infection
Test Window period Acute infection Asymptomatic inf ARC and AIDS
Antigen: p24, RT +* + - +
Virus isolation ++ ± - +
Antibody
ELISA test - + + +
Western blot test - + + +
Partial p24 and/or
gp 120
(Full pattern) (Absence of p24
antibody)
* Positive in less than 50% cases.
42. Laboratory Tests for Detection of Specific Antibodies in HIV
infection
1. Screening (E/R/S) tests
a) ELISA
b) Rapid tests
i. Dot blot assay
ii. Lateral flow assay (Immunochromatography)
iii. Particle agglutination (latex, gelatin)
iv. HIV spot and comb tests
c) Simple tests
a) These are based on ELISA principle
2. Supplemental tests
a) Western blot test
b) Indirect
imunofluorescence test
c) Radio Immuno
Precipitation assay
43. Western Blot
• Most popular confirmatory test.
• 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.
• 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.
44. Non-specific Tests
• Total and differential leucocyte count
– In AIDS, leucopenia with a lymphocyte count less than 400 per mm3.
• T-lymphocyte subset assays
– CD4:CD8 T-cell ration of 2:1, is reversed to 0.5:1 in cases of AIDS. The count of
CD4 lymphocytes falls below 200 per mm3.
• Platelet count
– Thrombocytopenia in AIDS patients
• IgG and IgA levels
– Levels of both are raised
• Skin test for CMI
– Diminished as evident from tuberculin test or other skin tests for CMI
47. Postexposure Prophylaxis (PEP)
Category of exposure Status of Source
HIV positive and
clinically
asymptomatic (Low
risk)
HIV positive and
clinically
symptomatic (High
risk)
HIV status
not known
(Unknown)
Mild exposure (Mucous membrane/ non-intact
skin with small volume)
Consider two drug
PEP regimen
Start two drug PEP
regimen
UsuallynoPEPor
considertwoPEP
regimen
Moderate exposure (Mucous membrane/non –
intact skin with large volume or percutaneous
superficial exposure with solid needle)
Start two drug PEP
regimen
Startthreedrug
PEPregimen
Severe exposure (Percutaneous with large
volume)
Start three drug PEP
regimen
48. • Zidovudine 300mg BD and Lamivudine 150mg BD are used in basic two drug
regimen.
• Expanded three drug PEP regimen, a protease inhibitor
– Lopinavir 400mg BD or 800mg OD or ritonavir 100 mg BD or 200 mg OD are
preferred as third drug.
• To be effective these drugs must be started within the first 72 hrs and ideally within
2 hrs.
• PEP should be continued for a period of 4 weeks.