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Hiv
1. RETROVIRUSES
• 1) INTRODUCTION :
• I) Reverse transcriptase
• Ii) 3 subfamily and seven genera: 2 genera pathogenic to human
• A) genus lenti virus : HIV 1& 2
• B)Deltaretrovirus: HTLV-1
2. • III) Types : based on transmission from 1 host to another : 2 types
• A) Exogenous retroviruses : spread horizontally 1 to other (HIV and HTLV-1)
• B) Endogenous retroviruses: vertically by integration the provirus into host
chromosome )
3. 2) HUMAN IMMUNODEFICANCY
VIRUS (HIV)
• i) History and origin
• a) Acquire immunodeficiency syndrome (AIDS)
• b) History : first case in new york (1981)
• c) acquired from chimpanzee
4. • Ii) Morphology:
• A) 80-110 nm
• B) Envelope: made up of
• i) lipid part : derived from host cell
• Ii) protein : 2 component
• A) glycoprotein 120 (gp 120)
• B) glycoprotein 41 (gp 41)
• C) Nucleocapsid: capsid (icosahedral) made up of core
protein
lipid
nucleoc
apsid
matrix
5. • i) RNA : two copy of positive sence ssRNA
• Ii) viral enzyme : RT , integrase and proteases (RNA)
6. • Ii) HIV Genes and Antigens:
• gag ,pol and env and 6 non structural or regulatory gene
• A) structural gene :
• i)gag gene :
• 1) cods for core and shell of virus
• 2) Express P55 protein (3 protein)
•
P18 : matrix and
cell
P24 and p15 : core
antigen
p18
p24
p15
7. • Ii) pol gene: codes for viral enzymes (rt , protease and
integrase)
• Iii) env gene: codes for envelope glycoprotein
P31
(integrase)
P51: rt
p66
Gp120(main
receptor protein)
for binding to CD4
Gp41 :
fusion
protein
8. • B) Non-structural gene : regulate
viral replication help viral
pathogenesis
• A) Tat : transcriptional transactivator
gene (HIV-1 replication)
• B) nef (negative factor gene):
regulate CD4 expression on cell
surface and increase infectivity
• C) rev (regulator of virus gene)
:enhances expression of structural
gene
• D) vif (viral infectivity factor) :
influences infectivity
• E) vpu gene: cd4 degeneration ,
release progency virus from host cells
and expressed only by HIV-1
9. • F) VPR: increase transport of viral genome into nucleus
• G) vpx: in HIV-2 only
10.
11. • Iii) Antigenic variation and Diversity :
• Extensive antigenic diversity high mutation
• Error prone nature of rt enzyme
• Mutation in any gene but (most common evn gene)
•
12. • Iv) Disinfection and inactivation:
• 1) Inactivated completely by
• A) 10% household bleach for 10 min (infected needle)
• B) Ethanol (50%) ,isopropenol (35%)
• C) lysol (0.5%) for 10 min
• D) para formaldehyde (0.5%) for 10 min
• E) h2o2 (0.3%) : 10 min
• F) heating serum 56oc : 10 min
• G) Ph :1.0 , 13.0
15. B) RECEPTOR ATTACHEMENT
CXCR4: T CELL
CCR5: MACROPHAGE
DENDRETIC CELL
SPECIFIC LECTINE
RECEPTOR
Mutation in CCR5 (Delta 32)
Inhibit entry of hiv
Fount in lucky person of
Europe and Western Asia
18. vi) DISEASE PROGRESSION
• A) factor effecting disease progression
• i) viral factor : viral fitness , co-receptor , escape mutation ,
latency
• Ii)host factor :genetic factor (polymorphism of HLA [HLA ,
A24 , B35 , B8 :RAPID and HLA –B27 and 57 -slow} and
chemokine receptor.
• Iii) Mutation in CCR5 coreceptor
19. • B) Natural course : 80-90 % people , survival time 10 years .
• Stages
• i) Acute HIV disease: hiv in LN , p. Viremia , flue like symptom (50-70%) ,
after 3-6 weeks significant drop in CD4 , Ab negative [window period] )
• Ii) Asymptomatic stage : cmi and hmi develope, viremia drop , CD4 count normal
, Ab appear , Last for 10 yrs ( few months to 30 yrs) , latancy broke (dead 2 yrs) if
untreated
• Iii) PGL: HIV multiply in lymphnode , enlarged lymphnode (>1cm) at 2 or more
sites , d/F other lymphadenitis by lymphomas
• Iv) symptomatic HIV infection : ( CD4 , diarrhoea [1 month] ,weight loss [>10%]
, fatigue , mailase , night sweat opportunistic infection)
• V) AIDS: CD4 , HIGH viral load , opportunistic infections
36. • 1) HIV/AIDS situation in India :
• 2015 in India: 0.26 (0.3% -male , 0.22-female)
• PLHA: 2.1 million
• PHLHA: Andhra Pradesh , Maharashtra , and Karnataka
• Prevalence :nagaland , Migoram , and Manipur
•
37. • 2) Reservoir: Human
• 3) AIDS control organisation :
• A) the joint united Nations program on HIV and AIDS (UNAID)
• B) National AIDS control program
• C) State AIDS prevention and control society (SACS)
38. • IX) IMMUNE RESPONCE :
• 1) viremia :soon after infection
• 2)Humoral response : IgM , IgA and IgA against structural protein ,
regulatory and accessory proteins
• 3) Window period : interval b/n onset of infection till production of Ab (3-
12 weeks)
• 3)Ab to gag appear first , env and pol (simultaneously)
39. • 4) As infection progression , Ab to P24 Decline as p24 antigen raised
• 5) IgG : Long lasting
• 6) IgM : appear earlier (2-11 days –needle stick injury , infection in
newborn)
• 7) IgA: Serum and mucous secretion
•
40. ix) Laboratory Diagnosis
• 1) Moral , ethical , legal and physical issue (positive case)
• 2) 3cs should be taken while performance test.
• A) consent : patient should be explained about nature of test
• B) Confidentiality : patient name and HIV positive should not be
mentioned on report form
• C) counselling : to motivate the individual and tell spouse to induce
behavioural change .
46. • Iii) Rapid test:
• A) dot blot assay : immunochromatography
47. • IV) Detection of p24 core antigen:
• Detectable 12-26 days (infection)
• Last (3-4weeks)
• Detected by 4th generation
• Less sensitive: once Ab formed , binds to it and Ab and Ag complex
eliminate from blood
48. • V) Viral RNA Detection : gold standard method
• A) rtpcr , Branch DNA assay , NASBA
• B) Best method for detection during window period
• C) detect very earlier than others methods
52. • 2 DRUG REGIMENT :ZIDOVUDINE 300 mg BD and lamivudine 150
mg BD
• 3 DRUG PPE REGIMENT : ZIDOVUDINE 300 mg BD and lamivudine
150 mg BD AND LOPINA VIR 400 mg BD AND RITONAVIR 100 mg
BD
