INTRODUCTION
• Family- Retroviridae
•Subfamily- Orthoretrovirinae
• Genus- Lentivirus
• Species- HIV1 and HIV2
• HIV1- isolated in America, Europe, central
Africa
• HIV2-in west Africa, less virulent and spread
is not as widely and rapidly as HIV 1
• In India, HIV 1 subtype C is the most popular
CP baveja – Textbook Of Microbiology – 5th Edition
3.
SUBTYPES OF HIVVIRUS
CP baveja – Textbook Of Microbiology – 5th Edition
4.
MORPHOLOGY
• Spherical envelopedvirus, 90-120nm in
diameter
• Has 2 identical copies of ssRNA genome
• Virus core- surrounded by nucleocapsid
composed of protein
• Envelope- made of lipoprotein
• Major virus coded envelope glycoproteins-
projects as spikes on surface and anchor
transmembrane pedicles
CP baveja – Textbook Of Microbiology – 5th Edition
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Mode of transmission
•1) Sexual contact (86%): most common mode, occurs among both
homosexual and heterosexual individual.
• 2) Parenteral transmission (89%)- via blood after receiving infected
blood transfusions, blood products, sharing contaminated syringes and
needles as intravenous drug abusers or accidental inoculation.
• 3) Perinatal transmission / Vertical transmission(93%)– transmitted
from infected mother to her child transplacentally or perinatally.
CP baveja – Textbook Of Microbiology – 5th Edition
1. GROUP 1-Acute HIV infections- characterized by acute onset of fever, malaise, sore
throat, myalgia, arthralgia, skin rash an lymphadenopathy.
2. GROUP 2- Asymptomatic infection – infected persons are usually well but show
positve hiv antibody tests and are infectious.
3. GROUP 3- Persistent generalised lymphadenopathy- characterised by enlarged
lymph nodes.
4. GROUP 4- Symptomatic HIV infection- CD4+ T lymphocyte count falls below 400
per mm cube, followed by symptoms like fever, diarrhoea, weight loss, night sweats
and opportunistic infections.
When CD4+ cells fall below 200 per mm cube, titer of virus increases markedly and
there is irreversible breakdown of immune defence mechanisms
Aids is the end stage of HIV infection
CP baveja – Textbook Of Microbiology – 5th Edition
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WHO CLASSIFICATION
1. Stage1: Asymptomatic or Persistent Generalized Lymphadenopathy
Patients in this stage may be asymptomatic or have persistent generalized
lymphadenopathy (swollen lymph nodes) for more than six months.
2. Stage 2: Mildly Symptomatic
Characterized by mild symptoms like unexplained moderate weight loss, recurrent
respiratory infections (sinusitis, bronchitis, etc.), or certain skin conditions (herpes zoster,
angular cheilitis, etc.).
3. Stage 3: Moderately Symptomatic
Includes conditions where a presumptive diagnosis can be made based on clinical signs
or simple tests, such as severe weight loss, unexplained anemia, or neutropenia.
4. Stage 4: AIDS
This stage is characterized by severe symptoms and the presence of opportunistic
infections that indicate advanced HIV disease.
12.
LABORATORY DIAGNOSIS
• 1)Specific tests for HIV infections
• A) Antigen detection: p24 is earliest virus marker to appear in blood, useful for diagnosis in
window period
• B) Virus isolation: isolated from CD4+ lymphocytes of peripheral blood, bone marrow, and
serum, important test for diagnosis in window period when antibodies are absent in serum
• C) Detection of viral nucleic acid: viral nucleic acid is diagnosed by PCR, test is highly sensitive
and specific, used for diagnosis in window period
• D) Antibody detection: demonstration of antibodies is simplest and most commonly used
technique, may take several weeks to months for antibodies to appear after infection, IGM
antibodies appear firs in 3-4 weeks after infection followed by IGG
HIV infected persons remain negative for antibodies during window period ( here initial viral
replication takes place for 2-3 weeks)
CP baveja – Textbook Of Microbiology – 5th Edition
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• 2 screeningtests
• A) ELISA: most commonly used, highly sensitive and specific,
here saliva is acceptable alternative to serum for antibody
testing
• B) Rapid tests: test takes less than 30 mins and do not require
expensive equipment, includes dot-blot assay, particle
agglutination and hiv spot and comb tests
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• 3 supplementaltests
• A) Western Blot test- hiv proteins are separated by polyacrylamide gel
electrophoresis, separated proteins are blotted onto strips pf
nitrocellulose paper. These strips are reacted with test sera,
antibodies to hiv proteins if present in test serum, combine with
fragments of hiv. Position of colour band on strip fragment of
antigen with which antibodies have reacted.
- Positive result is confirmed after retesting the original
- Test is cumbersome, expensive and not readily available
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• B) Indirectimmunofluorescence test: hivinfected cells are fixed onto glass slides
and then reacted with serum followed by fluorescein conjugated antihuman
gamma globulin
- Positve result apple green fluorescence
Other non-specific tests
• 1) TLC and DLC: there is leucopenia with lymphocyte count less than 400 per mm
cube
• 2) T-lymphocyte subset assay: normal cd4: cd8+ t cell ratio is 2:1 but here it is
reveresed to 0.5:1, as cd4+ lymphocyte counts fall below 200 per mm cube
CP baveja – Textbook Of Microbiology – 5th Edition
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PREVENTION
• 1) Sexualcontact use of physical barriers can prevent transmission of
virus
• 2) Sharing needles contaminated syringes or needles should not be
shared
• 3) Blood all blood and blood products should be screened, and same
applies for donation of cornea, semen, marrow, kidney and other
organs
• 4) Isolation of aids patient and initiation of treatment
• 5) Control of infection screening of individuals within risk groups
helps to identify HIV infected persons
CP baveja – Textbook Of Microbiology – 5th Edition
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ANTIRETROVIRAL THERAPY
• Highlyactive antiretroviral therapy is effective in inhibition of hiv
replication in hiv-infected individuals
• These drugs include both nucleoside and non nucleoside inhibitors of
enzyme reverse transcriptase , viral protease inhibitor, fusion
inhibitor, integrase inhibitor and entry inhibitor
• These drugs can be used as monotherapy or in various combinations
CP baveja – Textbook Of Microbiology – 5th Edition
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POST EXPOSURE PROPHYLAXIS
•Exposure to blood, body fluid, other potentially infected material or an
instrument contaminated may lead to risk of acquiring HIV
• Following exposure, postexposure prophylaxis may be required
depending upon category of exposure and hiv status of exposure source
• Zidovudine 300mg and lamivudine 150 mg bd are 2 basic drugs in this
regimen
• 3 drug PEP regimen: Lopinavir 400mg BD/ 800mg OD or Ritonavir 100
mg BD/200mg OD can be added as 3rd
drug
• To be effective start these drugs within first 72 hrs and ideally within
2 hrs, followed through 4 weeks
CP baveja – Textbook Of Microbiology – 5th Edition
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NEEDLE STICK INJURIES
•Needle stick injury poses as a major risk factor
among dentists for HIV transmission.
• It can occur during recapping of needles, while
administering local anesthetics, disposing of
needles, handling of trash.
• Chances of transmission through NSI is 0.3%.
• Ensure proper handling, recapping and
segregation of needles.
20.
UNIVERSAL PRECAUTIONS
• Assumeall specimens / patients are potentially infectious for hiv and other blood borne
pathogens
• All blood specimens/ body fluids should be placed in leak proof impervious bags for
transportation to labs
• Use gloves while handling blood and body fluid specimens and other objects exposed to them, if
there’s chance for splattering wear – facemask with googles
• Wear lab coats or gowns while working in labs, and these should not be taken outside
• Never pipette with mouth
• Decontaminate lab surfaces with appropriate disinfectant after blood spillage and when
procedures complete
• Limit use of needles and syringes to situations for which there are no other alternatives
• Biological safety hoods to be used
• All potentially contaminated materials of labs to be decontaminated before disposal
• Always wash hands after lab work and remove all protective clothing’s before leaving labs
CP baveja – Textbook Of Microbiology – 5th Edition
#6 Entry:HIV attaches to and enters a CD4+ T cell, facilitated by viral proteins like gp120 and gp41, which bind to CD4 receptors and co-receptors on the cell surface.
2. Uncoating:Inside the cell, the viral envelope and capsid break down, releasing the viral RNA and enzymes like reverse transcriptase, integrase, and protease.
3. Reverse Transcription:The viral RNA is converted to DNA by reverse transcriptase. This process is prone to errors, leading to mutations.
4. Integration:The viral DNA is inserted into the host cell's genome by integrase, creating a provirus.
5. Replication (Transcription & Translation):The host cell's machinery transcribes the provirus into new HIV RNA and uses this RNA to produce viral proteins.
6. Assembly:The new viral RNA and proteins move to the cell surface, where they assemble to form new HIV particles.
7. Budding and Maturation:The immature HIV buds off from the cell, acquiring a lipid membrane from the host cell. HIV protease then cleaves the viral proteins, creating a mature, infectious virus.
#7 HIV INFECTS ALL CELLS EXPRESSING AT THEIR SURFACE THE CD4 ANTIGEN WHICH IS THE RECEPTOR FOR VIRUS
IT INFECTS PRIMARILY CD4+ LYMPHOCYTES
#9 The system categorizes individuals into stages based on the presence or absence of HIV-related symptoms and conditions, ranging from asymptomatic infection to advanced AIDS.
#10 - HERPES SIMPLEX INFECTIONS MAYBE PRESENTED WITH MULTIPLE, DEEPER, MORE PAINFUL ORAL LESIONS IN PATIENTS WITH AIDS, AND HEAL SLOWER
- THRUSH IS USUALLY FOUND ON PALATAL AND BUCCLA MUCOSAE
- ASYMPTOMATIC ERYTHEMATOUS LESIONS OF CANDIDAE MAY ALSO APPEAR
#12 VIRUS ISOLATION- FOR DIAGNOSIS, VIRUS IS NOT ROUTINELY ISOLATED
#13 THERE ARE TWO TYPES OF SEROLOGICAL TESTS : SCREENING AND SUPPLEMENTAL TESTS