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EDUCATION
NATURAL HISTORY OF HIV
Natural Course of HIV Infection and Host Responses
HIV-CTL+CD8 activi
1000
900 Asymptomatic
800
CD4+ cell Count
CD4+ T cells
700 TB
Acute HIV
600 infection
syndrome
500
HZV
400 Relative level of OHL
300 Plasma HIV-RNA
OC
200 PPE
PCP
100 TB CM
CMV, MAC
0
0 1 2 3 4 5 1 2 3 4 5 6 7 8 9 10 11
Months Years After HIV Infection
Oportunistic Infection
Pathogenesis of IRIS
Pathogenesis remains largely speculative
Current theories concerning pathogenesis are combination of
underlying antigenic burden, degree of immune restoration following
HAART and host genetic susceptibility.
These pathogenesis mechanism may interact and likely depend on
underlying burden of infection or noninfection agent.
Increased immune function (rapidly increased CD4 and decreased
Viral load)
Inflamatory reaction more likely to occur in patients low CD4 cont
(<50 copy) and high viral load (>100.000 copy)
High proliferation of Lymphonode
IRIS has 2 classification reaction :
1. Unmasking
2. Paradoxical
Some report frequent in PI treatment
Causes of IRIS
Infectious and non infectiuos causes of IRIS in HIV-infected patients
Mycobacteria : Autoimmune :
R i s k factors
Male sex
Younger age
Lower CD4 cell count at ART initiation
Higher RNA at ART initiation
Lower CD4 cell percentage at ART initiation
Lower CD4 : CD8 ratio at ART initition
More rapid initial fall in HIV RNA on ART
Antiretroviral nave at time of OI diagnosis
Shorter interval between OI theraphy initition and ART initition
Manifestation of IRIS
More than 75% patients symptomatic for IRIS ;
manifestation within 90 days after initition ART
60% of IRIS events are due to Mycobacterium
tuberculosis, Mycobacterium avium complex (MAC) or
Crytococcal disease
Symptoms vary from mild to severe
Common clinical manifestation depend on basic OI
Worsening of coexisting infection such as flare of
Hepatitis B or C
Management
IRIS may be mild and resolve without treatment
Continue ART if the patients can tolerate it. In severe cases (live
threatining) may be temporary interuption until of ART until the
patients is stable.
The consensus is that ART should not be stop in almost all cases of
paradoxical inflamation.
Treatment unmasked OI such TB,MAC and Crytococcal disesae
(meningitis).
Corticisteroid treatment to suppress exaggerated inflamatory
response for moderate and severe cases of IRIS
Prednison 0.5 mg/kg/day for 5-10 days.
Double-blind, placebo controlled trial people with TB-associated
IRIS to 4 meeks prednison (1.5 mgr/kg/day for 2 weeks then 0.75
mg/kg/day for 2 weeks), p =0.04.
Antiretroviral Drugs 2003
NsRTI NNRTI PI
zidovudine (ZDV) nevirapine (NVP) saquinavir (SQV)
didanosine (ddI) efavirenz (EFV) ritonavir (RTV)
zalcitabine (ddC) delavirdine (DLV) indinavir (IDV)