The document discusses AIDS and lentiviruses. It covers topics such as the origin of HIV from primate lentiviruses, the classification and properties of lentiviruses, HIV infections in humans including pathogenesis and pathology, virus receptors, and the roles of CD4 T lymphocytes, monocytes, macrophages, and lymphoid organs in HIV infection.
THE BASIC INFORMATION ABOUT WHAT IS HIV AND HOW IT DESTRUCT THE IMMUNE SYSTEM. THEN LEADS TO AIDS. PRESENTATION ALSO EXPLAINS THE DIAGNOSIS OF HIV, ITS TREATMENT
WHY WE DONT HAVE VACCINE FOR HIV AND WHAT ARE THE PRESENT SCENARIO OF VACCINE DEVELOPMENT..
I HOPE IT WILL EXPLAIN WELL ABOUT HIV INFECTION AND AIDS, MAY PROVE USEFUL FOR YOU GUYS.....
THE BASIC INFORMATION ABOUT WHAT IS HIV AND HOW IT DESTRUCT THE IMMUNE SYSTEM. THEN LEADS TO AIDS. PRESENTATION ALSO EXPLAINS THE DIAGNOSIS OF HIV, ITS TREATMENT
WHY WE DONT HAVE VACCINE FOR HIV AND WHAT ARE THE PRESENT SCENARIO OF VACCINE DEVELOPMENT..
I HOPE IT WILL EXPLAIN WELL ABOUT HIV INFECTION AND AIDS, MAY PROVE USEFUL FOR YOU GUYS.....
This powerpoint, deals with HIV pathophysiology, signs and symptoms, mode of transmission and diagnostic parameters.
Purely based on clinical pharmacist perspective.
This powerpoint, deals with HIV pathophysiology, signs and symptoms, mode of transmission and diagnostic parameters.
Purely based on clinical pharmacist perspective.
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.
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.
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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.
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
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
1. AIDS & Lentiviruses
Term: Spring 2020
Date:5th Nov, 2020
Lecturer: Mr. Kassim A. Jim’ale
Somali National University
Mogadishu, Somalia
2. Introduction
There are different Human immunodeficiency virus
(HIV) types
These viruses are derived from primate lentiviruses
These viruses are the etiologic agents of AIDS
The illness was first described in 1981
HIV-1 was isolated by the end of 1983
Since then, AIDS has become a worldwide epidemic,
expanding in scope and magnitude
HIV infections have affected different populations and
geographic regions
3. Introduction
Millions are now infected worldwide
Once infected, individuals remain infected for life
Within a decade, if left untreated:
The vast majority of HIV-infected individuals develop fatal
opportunistic infections as a result of HIV-induced deficiencies
in the immune system
AIDS is one of the most important public health problems
worldwide at the start of the 21st century
The development of highly active antiretroviral therapy
(HAART) for chronic suppression of HIV replication and
prevention of AIDS has been a major achievement in HIV
medicine
4. Properties of Lentiviruses
Virion: Spherical, 80–100 nm in diameter, cylindric core
Genome: Single-stranded RNA, linear, positive-sense, 9–10 kb
Proteins:
Envelope glycoprotein undergoes antigenic variation
Reverse transcriptase enzyme contained inside virions
Protease required for production of infectious virus
Envelope: Present
Replication:
Reverse transcriptase makes DNA copy from genomic RNA
Provirus DNA is template for viral RNA
Genetic variability is common
Maturation: Particles bud from plasma membrane
5. Properties of Lentiviruses
Outstanding characteristics:
Members are nononcogenic and may be cytocidal
Infect cells of the immune system
Proviruses remain permanently associated with cells
Viral expression is restricted in some cells in vivo
Cause slowly progressive, chronic diseases
Replication is usually species-specific
Group includes the causative agents of AIDS
6. Structure & Composition
HIV is a retrovirus, a member of the Lentivirus
genus
It exhibits many of the physicochemical features
typical of the family
The unique morphologic characteristic of HIV is:
A cylindrical nucleoid in the mature virion
The diagnostic bar-shaped nucleoid is visible in
electron micrographs in those extracellular particles
that happen to be sectioned at the appropriate angle
8. Classification
Lentiviruses have been isolated from many species
including more than two dozen different African
nonhuman primate species
There are two distinct types of human AIDS viruses:
HIV-1 and HIV-2
The two types are distinguished on the basis of:
Genome organization
Phylogenetic (evolutionary) relationships with other primate
lentiviruses
Sequence divergence between HIV-1 and HIV-2 exceeds
50%
9. Origin of AIDS
HIV in humans originated from cross-species
infections by simian viruses in rural Africa
Probably due to direct human contact with infected
primate blood
Current evidence is that the primate counterparts of
HIV-1 and HIV-2 were transmitted to humans on
multiple (at least seven) different occasions
10. Origin of AIDS
Sequence evolution analyses place the introduction of
SIVcpz into humans that gave rise to HIV-1 group M at
about 1930, although some estimates push the date back
to about 1908
Presumably, such transmissions occurred repeatedly
over the ages, but particular social, economic, and
behavioral changes that occurred in the mid 20th
century provided circumstances that allowed these virus
infections to expand, become well-established in
humans, and reach epidemic proportions
11. Disinfection & Inactivation
HIV is completely inactivated by treatment for 10 minutes at
room temperature with any of the following:
The virus is also inactivated by extremes of pH (pH 1.0, pH
13.0)
When HIV is present in clotted or unclotted blood in a needle
or syringe, exposure to undiluted bleach for at least 30
seconds is necessary for inactivation
bleach 50% ethanol
35% isopropanol 1% Nonidet P40
0.5% Lysol 0.5% paraformaldehyde
0.3% hydrogen peroxide
12. Disinfection & Inactivation
The virus is not inactivated by 2.5% Tween 20
Although paraformaldehyde inactivates virus free in
solution, it is not known if it penetrates tissues sufficiently
to inactivate all virus that might be present in cultured cells
or tissue specimens
HIV is readily inactivated in liquids or 10% serum by
heating at 56°C for 10 minutes, but dried proteinaceous
material affords marked protection
Lyophilized blood products would need to be heated at
68°C for 72 hours to ensure inactivation of contaminating
13. Animal Lentivirus Systems
Insights into the biologic characteristics of lentivirus infections
have been gained from experimental infections, including
sheep with visna virus
Natural disease patterns vary among species, but certain
common features are recognized
1. Viruses are transmitted by exchange of body fluids
2. Virus persists indefinitely in infected hosts, though it may be
present at very low levels
3. Viruses have high mutation rates, and different mutants will
be selected under different conditions (host factors, immune
responses, tissue types)
1. Infected hosts contain "swarms" of closely related viral
genomes, known as quasi species
14. Animal Lentivirus Systems
4. Virus infection progresses slowly through specific
stages
i. Cells in the macrophage lineage play central roles in the
infection
ii. Lentiviruses differ from other retroviruses in that they can
infect nondividing, terminally differentiated cells
iii. However, those cells must be activated before viral
replication ensues and progeny virus is produced
iv. Virus is cell-associated in monocytes and macrophages, but
only about one cell per million is infected
v. Monocytes carry the virus around the body in a form that the
immune system cannot recognize, seeding other tissues
vi. Lymphocyte-tropic strains of virus tend to cause highly
productive infections, whereas replication of macrophage-
15. Animal Lentivirus Systems
5. It may take years for disease to develop
i. Infected hosts usually make antibodies, but they do not
clear the infection, so virus persists lifelong
ii. New antigenic variants periodically arise in infected
hosts, with most mutations occurring in envelope
glycoproteins
iii. Clinical symptoms may develop at any time from 3
months to many years after infection
iv. The exceptions to long incubation periods for lentivirus
disease include AIDS in children, infectious anemia
in horses, and encephalitis in young goats
16. Animal Lentivirus Systems
Host factors important in pathogenesis of disease include:
A. Age (the young are at greater risk)
B. Stress (may trigger disease)
C. Genetics (certain breeds of animals are more susceptible)
D. Concurrent infections (may exacerbate disease or facilitate
virus transmission)
Simian lentiviruses share molecular and biologic
characteristics with HIV and cause an AIDS-like disease in
rhesus macaques
The SIV model is important for understanding disease
pathogenesis and developing vaccine and treatment
strategies
17. Virus Receptors
All primate lentiviruses use as a receptor:
The CD4 molecule, which is expressed on macrophages and T
lymphocytes
A second coreceptor in addition to CD4 is necessary for HIV-1 to gain
entry to cells
The second receptor is required for fusion of the virus with the cell
membrane
The virus first binds to CD4 and then to the coreceptor
These interactions cause conformational changes in the viral
envelope, activating the gp41 fusion peptide and triggering
membrane fusion
Chemokine receptors serve as HIV-1 second receptors
18. Virus Receptors
The chemokine receptors used by HIV for cell entry
are found on:
Lymphocytes, Macrophages, and Thymocytes as well
as on Neurons and cells in the colon and cervix
The requirement for a coreceptor for HIV fusion
with cells provided new targets for antiviral
therapeutic strategies
The first HIV entry inhibitor licensed in the United
States in 2003
19. HIV Infections in Humans: Pathogenesis
& Pathology
Overview of Course of HIV Infection
The typical course of untreated HIV infection spans about a decade
Stages include:
1. The primary infection
2. Dissemination of virus to lymphoid organs
3. Clinical latency
4. Elevated HIV expression
5. Clinical disease
6. Death
The duration between primary infection and progression to clinical
disease averages about 10 years
In untreated cases, death usually occurs within 2 years after the
onset of clinical symptoms
20. HIV Infections in Humans: Pathogenesis
& Pathology
Following primary infection, there is a 4 to 11day period between
mucosal infection and initial viremia
The viremia is detectable for about 8–12 weeks
Virus is widely disseminated throughout the body during this time, and
the lymphoid organs become seeded
An acute mononucleosis-like syndrome develops in many patients
(50–75%) 3–6 weeks after primary infection
There is a significant drop in numbers of circulating CD4 T cells at this
early time
An immune response to HIV occurs 1 week to 3 months after infection
A. Plasma viremia drops
B. Levels of CD4 cells rebound
However, the immune response is unable to clear the infection
completely, and HIV-infected cells persist in the lymph nodes
21. HIV Infections in Humans: Pathogenesis
& Pathology
This period of clinical latency may last for as long as 10 years
During this time, there is a high level of ongoing viral replication
It is estimated that 10 billion HIV particles are produced and
destroyed each day
The half-life of the virus in plasma is about 6 hours, and the virus
life cycle (from the time of infection of a cell to the production of new
progeny that infect the next cell) averages 2.6 days
CD4 T lymphocytes, major targets responsible for virus production,
appear to have similar high turnover rates
Once productively infected, the half-life of a CD4 lymphocyte is about
1.6 days
Because of this rapid viral proliferation and the inherent error rate of
the HIV reverse transcriptase, it is estimated that every nucleotide
of the HIV genome probably mutates on a daily basis
22. HIV Infections in Humans: Pathogenesis
& Pathology
Eventually, the patient will develop constitutional
symptoms and clinically apparent disease, such as
opportunistic infections or neoplasms
Higher levels of virus are readily detectable in the plasma
during the advanced stages of infection
HIV found in patients with late-stage disease is usually
much more virulent and cytopathic than the strains of
virus found early in infection
Often, a shift from monocyte-tropic or macrophage-
tropic (M-tropic) strains of HIV-1 to lymphocyte-tropic
(T-tropic) variants accompanies progression to AIDS
24. CD4 T Lymphocytes, Memory Cells, &
Latency
The cardinal feature of HIV infection is the depletion of T
helper-inducer lymphocytes
—the result of HIV replication in this population of lymphocytes
as well as of the death of uninfected T cells by indirect
mechanisms
The T-cells express the CD4 phenotypic marker on their
surface
The CD4 molecule is the major receptor for HIV
It has a high affinity for the viral envelope
The HIV coreceptor on lymphocytes is the CXCR4
chemokine receptor
25. CD4 T Lymphocytes, Memory Cells, &
Latency
Early in infection, primary HIV isolates are M-tropic
However, all strains of HIV infect primary CD4 T lymphocytes
As the infection progresses, the dominant M-tropic viruses are replaced by T-
tropic viruses
The consequences of CD4 T cell dysfunction caused by HIV infection are
devastating
This is because the CD4 T lymphocyte plays a critical role in the human immune
response
It is responsible directly or indirectly for induction of a wide array of lymphoid and
nonlymphoid cell functions
These effects include:
Activation of macrophages
Induction of functions of cytotoxic T cells, natural killer cells, and B cells
Secretion of a variety of soluble factors that induce growth and differentiation of
26. CD4 T Lymphocytes, Memory Cells, &
Latency
At any given time, only a small fraction of CD4 T cells are productively
infected
Many infected T cells are killed, but a fraction survives and reverts to a
resting memory state
There is little or no virus gene expression in the memory cells, and they
provide a long-term, stable latent reservoir for the virus
Less than 1 cell per million resting CD4 T cells harbor latent HIV-1
provirus in patients on successful antiretroviral therapy
Even after 10 years of treatment, patients show very little change in
the size of the latent HIV reservoir because the latent reservoir of
infected memory cells decays very slowly
27. CD4 T Lymphocytes, Memory Cells, &
Latency
It is unlikely that an HIV infection can be cured
If there were a million infected memory cells in the body, it would
take about 70 years for them to decay
When exposed to antigen or when drug therapy is
discontinued, the memory cells become activated and
release infectious virus
It is possible that other drug-insensitive reservoirs may
also exist among macrophages, hematopoietic stem
cells, or brain cells
28. Monocytes & Macrophages
Monocytes and macrophages play a major role in the
dissemination and pathogenesis of HIV infection
Certain subsets of monocytes express the CD4 surface
antigen and therefore bind to the envelope of HIV
The HIV coreceptor on monocytes and macrophages is the
CCR5 chemokine receptor
In the brain, the major cell types infected with HIV appear to
be the monocytes and macrophages, and this may have
important consequences for the development of
neuropsychiatric manifestations associated with HIV
infection
Infected pulmonary alveolar macrophages may play a role
in the interstitial pneumonitis seen in certain patients with
AIDS
29. Monocytes & Macrophages
Macrophage-tropic strains of HIV predominate
early after infection, and these strains are
responsible for initial infections even when the
transmitting source contains both M-tropic and T-
tropic viruses
It is believed that monocytes and macrophages
serve as major reservoirs for HIV in the body
These cells also aid dissemination of the virus in to
various organs of the body
30. Lymphoid Organs
Lymphoid organs play a central role in HIV infection
Lymphocytes in the peripheral blood represent only about 2% of the total
lymphocyte pool, the remainder being located chiefly in lymphoid organs
It is in the lymphoid organs that specific immune responses are generated
The network of follicular dendritic cells in the germinal centers of lymph
nodes traps antigens and stimulates an immune response
Throughout the course of untreated infection—even during the stage of
clinical latency—HIV is actively replicating in lymphoid tissues
The microenvironment of the lymph node is ideal for the establishment
and spread of HIV infection
Cytokines are released, activating a large pool of CD4 T cells that are highly
susceptible to HIV infection
As the late stages of HIV disease progress, the architecture of the lymph
nodes becomes disrupted
31. Neural Cells
Neurologic abnormalities are common in late stages of infection and are an AIDS-
defining condition
Central nervous system disease occurs to varying degrees in 40–90% of patients.
These include:
HIV encephalopathy
Peripheral neuropathies, and
Most serious—AIDS dementia complex
Both direct and indirect pathogenic mechanisms might explain the
neuropsychiatric manifestations of HIV infection
The predominant cell types in the brain that are infected with HIV are monocytes
and macrophages
Virus may enter the brain through infected monocytes and release cytokines that
are toxic to neurons as well as chemotactic factors that lead to infiltration of the
brain with inflammatory cells
HIV is present rarely, if at all, in neurons, oligodendrocytes, and astrocytes