All topics required for the BDS students in the chapter "RETROVIRUSES: HIV" is included in this ppt in a short and concise manner for better understanding. Please go through your books and use this ppt for revision purposes.

1. GAYATHRI M. NAIR

2. INTRODUCTION
RETROVIRUS • FAMILY: Retroviridae
Possess
TRANSCRIPTASE
• Characteristic feature
• RNA directed DNA polymerase
• Prepares DNA copy of RNA genome
• Takes place in host cell
e.g.: Human Immunodeficiency Virus
Rous Sarcoma Virus

3. REVERSE TRANSCRIPTION
GAYATHRI M. NAIR

4. MORPHOLOGY OF HIV
1. Spherical enveloped virus.
2. DIAMETER: 90-120nm.
3. Two identical copies of ssRNA genome.
4. Reverse Transcriptase present.
5. Virus core surrounded by nucleocapsid (made of
proteins).
6. Contains a lipoprotein envelope.
Major virus envelope glycoproteins
Projecting spikes
(on the surface)
Anchoring transmembrane
pedicle
GAYATHRI M. NAIR

5. Human
Immunodeficiency
Virus
HIV-1 HIV-2
1. Most common type of HIV
and accounts for 95% of all
infections.
2. Isolated in America,
Europe, Central Africa.
3. More fatal; progresses at
a faster rate.
1. HIV-2 is relatively uncommon
and less infectious.
2. HIV-2 is mainly concentrated
in West Africa and the
surrounding countries.
3. HIV-2 is less fatal and
progresses more slowly than
HIV-1.

6. MODES OF TRANSMISSION
1. Sexual
contact
*most important mode of
transmission.
*occurs among both
homosexual and
heterosexual individuals.
2. Parenteral
Transmission
*may occur through:
1. Infected blood
transfusion
2. Blood products
3. Sharing contaminated
syringes & needles
3. Perinatal
Transmission
*mother to child ----
transplacentally/
perinatally
GAYATHRI M. NAIR

7. CLASSIFICATION OF HIV INFECTION AND AIDS
HIV infection and AIDS
GROUP I
Acute HIV
infection
GROUP II
Asymptomatic
Infection
GROUP III
Persistent
Generalised
Lymphadenopathy
GROUP IV
Subgroup A
(Constitutional disease – ARC)
Subgroup B
(Neurological diseases)
Subgroup C
(Secondary infectious diseases)
Subgroup D
(Secondary cancers)
Subgroup E
(Other Conditions)
Symptoms:
• Fever
• Malaise
• Sore throat
• Myalgia
• Arthralgia
• Skin rash
• lymphadenopathy
• Usually well
persons
• Positive
antibody tests
• Infectious
• Enlarged
lymph nodes
present
• Lymphocyte counts fall below 400/mm3
• Symptoms: fever, diarrhoea, weight
loss, night sweats, opportunistic
infections
GAYATHRI M. NAIR

8. Clinical Features
Infects cells with surface antigen CD-4 (Receptor for HIV)
Primarily infects CD4+ lymphocytes.
CD4+ cells fall bellow 200/mm3
Virus increase markedly
Breakdown of immune defence mechanisms.
Mostly, patient dies of opportunistic infections.
AIDS IS THE END STAGE OF HIV INFECTIONS.

9. Opportunistic Infections and Malignancies Commonly Associated
with HIV Infection.
 Bacterial
1. Mycobacterial infections - Tuberculosis and non-tuberculous infections
2. 2. M. avium complex
3. 3. Salmonellosis.
 Viral
1. CMV
2. Herpes simplex
3. Varicella-zoster
4. Epstein-Barr (EB) virus
 Mycotic
1. Pneumocystis jiroveci pneumonia
2. Candidiasis
3. Cryptococcosis
4. Aspergillosis
5. Histoplasmosis
6. Coccidioidomycosis

10.  Parasitic
1. Toxoplasmosis
2. Cryptosporidiosis
3. Isosporiasis
4. Generalised strongyloidiasis
 Malignancies
1. Kaposi's sarcoma
2. B-cell lymphoma or non-Hodgkin's lymphoma

11.  Kaposi sarcoma (KS) is a cancer that causes patches of abnormal tissue
to grow under the skin, in the lining of the mouth, nose, and throat, in
lymph nodes, or in other organs. These patches, or lesions, are usually red
or purple. They are made of cancer cells, blood vessels, and blood cells.

12. ORAL MANIFESTATIONS
IN AIDS
• Greater risk of bacterial, viral and fungal infections of mouth.
• Dental caries, gingivitis.
• Oral Indicator of AIDS: Acute necrotizing ulcerative gingivitis
• Herpes simplex infection multiple, deep, more painful oral lesions  heal slower
 as immunocompetent person.
• Hair leukoplakia  caused by EBV+Candida/papillomavirus lesions: bilateral,
white, soft, hairy projections on margins of tongue (less commonly: unilateral,
corrugated elsewhere on tongue)
• Candidiasis in most patients.
• Angular chelitis
• Mucocutaneous candidiasis.
GAYATHRI M. NAIR

13. Acute necrotizing
ulcerative gingivitis Hair leukoplakia
Oral lesions of herpes
simplex infections
GAYATHRI M. NAIR

14. Mucocutaneous
Candidiasis Candidiasis Angular chelitis
GAYATHRI M. NAIR

15. LABORATORY
DIAGNOSIS Lab tests for specific
antibodies of HIV infection
Screening
Tests (E/R/S)
ELISA Rapid Tests
Dot Blot
assay
Particle
agglutination
HIV spot and
comb tests
Simple Tests
(Based on
principles of
ELISA)
Supplemental
Tests
Western blot
Indirect
immunofluoresecence test
Radio
Immuno
Precipitation
Assay
GAYATHRI M. NAIR

16. WESTERN BLOT
HIV proteins separated by polyacrylamide gel electrophoresis
Separated onto nitrocellulose paper
Paper reacted with test sera
Antibodies combine with HIV fragments
Position of colour bands determine fragment of reacted antigen
GAYATHRI M. NAIR

17. GAYATHRI M. NAIR

18. INDIRECT IMMUNOFLUORESCENCE TEST
Infected cells placed on slide
Reacted with sera
Reacted with fluorescent
antihuman gamma globulin
Apple green fluorescence
appears under microscope
Positive test
GAYATHRI M. NAIR

19. Prevention
• Sexual contacts: use of condoms.
• Sharing needles should be avoided.
• Blood & blood products should be screened for HIV.
• Immediate initiation of treatment.
• Identification of people under risk to identify
infected people.
GAYATHRI
M.
NAIR

20. PROPHYLAXIS
NO EFFECTIVE VACCINE
 HIGH MUTATION OF
VIRUS
GAYATHRI M. NAIR

21. ANTIRETROVIRAL THERAPY (ART)
HIGHLY ACTIVE ANTIRETROVIRAL THERAPY  Inhibition of HIV replication.
(HAART)
*major drawback: selection of resistant mutants*
Antiretroviral drugs include:
• Nucleoside and nucleotide inhibitors
• Viral protease inhibitors
• Fusion inhibitors
• Integrase inhibitors
• Entry inhibitors
ADR and high
cost restrict use
in developing
countries
GAYATHRI M. NAIR

22. Other measures in aids treatment include:
1. Treatment and prophylaxis of oppotunistic
infections and tumors
2. General management
3. Immunorestorative measures
GAYATHRI M. NAIR

23. POSTEXPOSURE PROPHYLAXIS
• TWO DRUG REGIMEN: Zidovudine 300mg (BD)
Lamivudine 500mg (BD)
• THREE DRUG REGIMEN: Zidovudine 300mg (BD)
Lamivudine 500mg (BD)
Lopinavir 400mg (BD)/ Retonovir 100mg(BD) {PROTEASE
INHIBITOR}
*effective only if started within 72hrs of exposure (ideally 2 hrs).
*continued for 4 weeks.
*antiseptics to be applied and site of injury to be washed thoroughly.
GAYATHRI M. NAIR

24. HOPE YOU UNDERSTOOD THE
TOPIC.
*Please go through your
textbooks thoroughly*
GAYATHRI M. NAIR

25. GAYATHRI M. NAIR