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HIV/ AIDS
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT: hermyc@live.com
OBJECTIVES
1.Introduction
2.Virology & Immunology
3.Natural history of HIV
4.Pathogenesis and Transmission
5.Lab Testing and Algorithm
6.Hiv & Tb
7..Oi’s
8.Art
9.Iris
910Art Resistance And Treatment Failure
11..Prevention
INTRODUCTION
 AIDS means Acquired Immunodeficiency
Syndrome
 HIV means Human immunodeffiency virus
HIV is the virus that causes immune
deficiency
 AIDS is the progression of HIV infection due to
destruction of immune system leading to
occurrence of diseases.
HIV
 HIV:Human Immunodeficiency Virus
 HIV is the virus that can ultimately lead to
AIDS
 HIV like other viruses needs to enter other
cells in order to replicate.
NATURAL HISTORY OF HIV INFECTION
VIROLOGY & IMMUNOLOGY:
 HIV is a single stranded RNA retrovirus from the
Lentivirus family.
 It consists of a cylindrical center surrounded by a
sphere shaped lipid envelope. The center consists
of 1 single strand with two molecules of RNA.
 The virus can use RNA & host’s DNA to make viral
DNA.
VIRAL GENES:
NAME OF GENE FUNCTIONS
LTR The Long Terminal Repeats are used for integration of the
virus into the host genome and also contain promoter and
enhancer sequences.
gag The Group-specific Antigen corresponds to the core and
capsid proteins.
pol: This gene encodes the reverse transcriptase, which actually
has several functions
env: This Envelope gene encodes the gp120 glycoprotein.
tat/rev This region encodes factors involved in transactivation and
other regulatory functions.
RETROVIRAL STRUCTURAL GENES
 gag = group specific antigen (internal structural proteins)
matrix (MA), binds envelope, organization
capsid (CA), protects genome and enzymes
nucleocapsid (NC) chaperones RNA, buds
 pol = polymerase enzymes
reverse transcriptase + RNA to DNA
RNAase H (RT) degrades template RNA
protease (PR) maturation of precursors
integrase (IN) provirus integration
 env = envelope proteins
surface glycoprotein (SU) receptor binding
transmembrane protein (TM) virus-cell fusion
CLASSIFICATION:
 Types
 HIV-1
 HIV-2
 HIV-1
Groups Subtypes Recombinants
Major (M) A,B,C,D,E,F,G,H,I,J AG,AE,AB,CRFs
Outlier (O)
Novel (N)
 HIV-2: 6 subtypes, A,B,C,D,E,F
 Jawetz Melnick and Adelberg. Medical Microbiology AIDS and Lentiviruses Mc Graw-
Education chpt 44 fourth ed 2007
MAJOR STEPS IN HIV LIFECYCLE
1. The virus attaches itself
to CD4+ T lymphocytes
2. Fusion and release of
RNA into the cytoplasm
3. Reverse transcription to
produce pro-viral DNA
4. Integration of pro-viral
DNA within host DNA
and synthesis of viral
proteins
5. Viral assembly and
release of mature
particles
LIFE CYCLE AND DRUGS
Warren Levinston review of medical microbiology and immunology, pathogenesis
and immunology Mc Graw-Education ed 13 pg 825 2014
IMMUNE SYSTEM/BODY DEFENCE
 Host defenses against viruses fall into two major
categories;
1.Nonspecific defenses;- interferons, natural killer
cells
2.Specifc defence ;-humoral, cell-mediated immunity
 NONSPECIFIC DEFENSES
Alpha and beta interferons are a proteins produced
by human cells after viral infection (or after
exposure to other inducers
They block the synthesis of viral proteins.
MECHANISM OF ON HOW THEY ACT
 One is a ribonuclease that degrades mRNA
 The other is a protein kinase that inhibits protein
synthesis.
 Interferons are divided into three groups based on the cell
of origin, namely, leukocyte, fibroblast, and lymphocyte,
They are also known as alpha, beta, and
gamma interferons, respectively
 Alpha and beta interferons are induced by viruses
PATHOGENESIS OF HIV INFECTION
HIV infection leads to profound
pathology, either directly, through
destruction of CD4+ T cells, other
immune cells, and neuroglial cells, or
indirectly, through the secondary
effects of CD4+ T-cell dysfunction and
resultant immunosuppression.
Once HIV has killed so many CD4+ T
cells that there are fewer than 200 of
these cells per microliter (µL) of blood,
1.HUMAN IMMUNODEFICIENCY
VIRUS -MEDIATED INHIBITION OF
HEMATOPOIESIS.-
-failure of normal hematopoiesis is
an obvious candidate mechanism to
account for depletion of CD4+T cells
during HIV infection
2.AUTOIMMUNITY-molecular
mimicry between HIV-1 envelope
constituents and host proteins lead
to pathogenic autoimmunity → cell
death.
3.INNOCENT BYSTANDERS.
Uninfected cells may die in an
innocent bystander scenario:
HIV particles may bind to the cell
surface, giving them the
appearance of an infected cell
and marking them for destruction
by killer T cells (cellular immune
response).
4.SYNCYTIA FORMATION. Infected
cells also may fuse with nearby
uninfected cells through CD4-mediated
fusion, forming balloon
(multinucleared)-like giant cells called
syncytia.
This mechanism of cell-to-cell spread
of HIV has been associated with the
death of uninfected cells. The
presence of syncytia-inducing
variants of HIV has been correlated
with rapid disease progression in
HIV-infected individuals.
PATHOGENESIS CONT…..
5.APOPTOSIS and Pyoptosis. Infected
CD4+ T cells may be killed when cellular
regulation is distorted by HIV proteins,
probably leading to their suicide by a
process known as programmed cell
death or apoptosis mediated by
caspase3.
-Uninfected cells also may undergo
apoptosis.
-Investigators have shown in cell
cultures that the HIV envelope alone or
bound to antibodies sends an
inappropriate signal to CD8+ T cells
causing them to undergo apoptosis
even though not infected by HIV.
PYROPTOSIS
 It has been known for some time now that apoptosis is a major
factor contributing to T-cell depletion, mediated by caspase-3, in
T-cells that are permissive to infection by HIV. However, there are
subsets of T-cells (abortive T-cells) that are non-permissive and
do not support HIV replication. In this subset of cells, cell death
occurs through a process called pyroptosis, driven by caspase-1
 Pyroptosis is a highly inflammatory form of programmed cell
death in which the dying cell releases all its cytoplasmic contents,
including inflammatory cytokines; these cytokines in turn trigger
pyroptosis in other T-cells as part of a vicious cycle of abortive T-
cell depletion
6.DIRECT CELL KILLING. Infected
CD4+ T cells may be killed directly
when large amounts of virus are
produced and bud off from the cell
surface, disrupting the cell
membrane, or
when viral proteins(gp120) and
nucleic acids collect inside the
cell, interfering with cellular
machinery → cell death.
 Regulatory T-Cells (Treg)
 Chronic immune Activation
 immune Activation and inflammation
-Cytikine storm,il 2 inhibited hence no maturation of
t cells
RISK FACTORS FOR HIV IN THE
GENERAL POPULATION
TRANSMISSION
1.MEN WHO HAVE SEX WITH MEN Study
done in Dar es Salaam, Tanzania by Nyoni and Ross in 2013
found that condom usage was very low among the MSM,
another study in Zanzibar 85% of the respondents reported
inconsistent condom use(M. Dahoma, L. et al 2011.Prevalence
(22-42%) (Leshabari et al. A Prevalence of the Human Immunodeficiency
Virus, other sexually transmitted infections, and health-related perceptions,
reflections, experiences and practices among men having sex with men in Dar
2013)
2.FEMALE SEX WORKERS mobile populations and sex
workers Prevalence 14-35%)(National AIDS Control Programme; A study
of Female Sex Workers in seven Regions: Dar es Salaam, Iringa, Mbeya, Mwanza,
Shinyanga, Tabora and Mara. A Report published in 2014 (ISBN 978-9987-650-83-5)
RISK FACTORS FOR HIV IN THE
GENERAL POPULATION CONT…..
3.PEOPLE WHO INJECT DRUGS (PWID).
PWID and their partners represent another population that can
serveas a “bridging population” for HIV transmission.
prevalence 16-51%(Dar es salaam. Integrated Bio-Behavioural Survey
Among People Who Inject Drugs in Dar es Salaam. April 16, 2014)
4.MOBILE POPULATION like,fishermen, prisoners and truck
drivers (Anthony Kapesa1 et al 2018) bridging population.
RISK FACTORS FOR HIV IN THE GENERAL
POPULATION CONT…..
 The prevalence of HIV among young people aged 15-
19 years was 1% (1.3% among girls, and 0.8%
among boys). Furthermore, the percentage of
women aged 20-24 infected with HIV is higher (4.4%)
than that of men (1.7%) in the same age
group.(National Bureau of Statistics, ICF International. Tanzania HIV AND AIDS
and Malaria Indicator Survey 2011-12. Dar es Salaam, March 2013).
 Women are disproportionally more affected, with an
HIV prevalence of 6.3 % versus 3.9% among men.
(THMIS 2011-12).
PREVENTION OF HIV INFECTION
1.MOTHER-TO-CHILD
TRANSMISSION OF
HIV( PMTCT) during,
labour, delivery or
breastfeeding ranges from
15% to 45%. PMTCT)
interventions can reduce this
risk to below 5%
(World Health Organization
(WHO) 'Mother-to-child
transmission of
HIV' [accessed November
2018])
2.PRE EXPOSURE PROPHYLAXIS (PREP)
POST EXPOSURE PROPHYLAXIS (PEP)
 PrEP. Prevent by 70%(Virginia A Fonner et al 2016 Jul.)
 Populations targeted for PrEP include Sex workers, Men who
have sex with men, People who inject drugs, Vulnerable
adolescent girls (15-19) and Young women (20-24) and Sero-
discordant couples. The
recommended PrEP regimen in Tanzania is:
Emtricitabine (FTC) 200 mg/Tenofovir Disoproxil Fumarate
(TDF) 300 mg (Truvada) PO Daily.
PEP.The guidelines recommend the use of TLD
(TDF+3TC/FTC+DTG) for adults and adolescents
3.VOLUNTARY MEDICAL MALE CIRCUMCISION
(VMMC) reduces female-to-male sexual
transmission of HIV by 60%.(Auvert, B et al.
(2005)
In Tanzania, the national prevalence of
male circumcision 77.6% among male
aged 15 years and older (THIS 16/17)
TESTING ALGORITHM
LABORATORY DIAGNOSTICS IN HIV
INFECTION
Antibody detection using rapid
tests/ELISA
Virological tests
Assays to detect p24 antigen
Assays to detect HIV DNA or RNA
(PCR)
Viral culture
LABORATORY DIAGNOSTICS IN HIV
INFECTION CONT........................
Antibody methods for diagnosing HIV
include:
 Rapid tests
 Enzyme Linked Immunosorbent Assay
(ELISA)
 Western Blot (confirmatory test if available)
Effective 12 weeks after infection, as
antibodies appear 6 to 12 weeks following
HIV infection in a majority of patients
Not suitable for use in infants under 18
months (use PCR)
LABORATORY DIAGNOSTICS IN HIV
INFECTION CONT.....
p24 tests
Detect the p24 antigen.
Based on the detection of antibodies
against HIV-1 antigens in serum.
Can be effective 2 to 3 weeks after
HIV infection.
Detect HIV antigen before antibody
can be detected.
LABORATORY DIAGNOSTICS IN HIV
INFECTION CONT........
DNA PCR tests
Useful in early diagnosis and infant
diagnosis (<18 months)
TB/HIV CO-INFECTION
Tuberculosis (TB) is a disease caused by
a bacterium called Mycobacterium
tuberculosis.
TB is spread by airborne route: droplet
nuclei
When a person with TB disease of the
lungs coughs or speaks, droplets of TB
bacteria spread through the air.
Once in the body, TB can be inactive or
THE IMAGE BELOW SHOWS THE DIFFERENCE
BETWEEN LATENT TB INFECTION AND TB DISEASE
TB/HIV CO-INFECTION CONT......
When the TB bacterium is inactive,
this is called Latent TB infection.
When the TB bacterium is active, this
is called TB disease.
Most exposed people do not become
infected.
Persons co-infected with HIV and TB
have highest risk for developing TB
disease
TB/HIV CO-INFECTION
CONT......
 The lifetime risk of developing activeTB among people
living with HIV (PLHIV) maybe 20 times higher than in
people without HIV [Organization WH. Global report TB 2015].
 Tanzania is among the 30 countries with high TB burden
and TB and HIV co-infection in the world.
[Organization WH. Global tuberculosis report 2018]
 Despite the increased access to antiretroviral therapy
(ART), mortality in PLHIV is still high, and TB is the leading
cause of mortality[Lawn SD,et al 2008]’
 Some studies found that TBpreventive therapy by isoniazid
reduces the incidence of TB in HIV-infected
Patients.(Mwinga A et all 1999)
TB/HIV CO-INFECTION CONT......
 Impact of HIV on TB:
 HIV is a high risk factor for the development of TB
 HIV increases risk of recurrent TB
 HIV promotes progression to active TB in people with
both recently acquired and latent M. tuberculosis
 Impact of TB on HIV:
 TB is the leading cause of death among PLHIV
 TB increases the risk of progression from HIV to AIDS
 TB is the most common OI in HIV infected people
TB/HIV CO-INFECTION CONT......
Clinical presentation
Atypical presentation of pulmonary
disease
Extra-pulmonary manifestations
Diagnosis of TB
More smear negative (low bacterial
load)
HIV positive persons are more likely
to have a negative TB skin test due
to skin test anergy (especially if CD4
is low)
Characteristics 2011 2012 2013 2014 Total
Overall 8765 (2.1) 9798 (2.3) 11,212 (2.5) 9857
(1.9)
39,632 (2.2)
Age group
< 15 years 687 (2.1) 784 (2.3) 1066 (3.2) 854
(2.4)
3391
(2.5)
≥ 15 years 8078
(2.1)
9014 (2.3) 10,146 (2.4) 9003
(1.9)
36,241 (2.2)
Sex
Male 3858 (2.9) 4474 (3.2) 5066 (3.5) 4681
(2.8)
18,079 (3.1)
Female 4907 (1.8) 5324 (1.8) 6146 (2.0) 5176
(1.5)
21,553 (1.7)
ART status
ART 1145 (1.5) 883 (1.4) 630 (1.2) 699
(1.2)
3357 (1.3)
Non-ART 7620 (2.3) 8915 (2.4) 10,582 (2.6) 9158 36,275 (2.3)
Table 2 Prevalence of TB among individuals enrolled in HIV care,
treatment, and support program in Tanzania from 2011 to 2014. . Majigo et
al. 2020
Variable TB cases 1000 person-years
TB incident rate
Overall 22,071 1323.6 16.7 (16.4–16.9)
Year of diagnosis
2011 5366 316.2 17.0 (16.5–17.4)
2012 5254 317.9 16.5 (16.1–17.0)
2013 6356 348.5 18.2 (17.8–18.7)
2014 5095 342.3 14.9 (14.5–15.4)
Sex
Male 9306 407.7 22.8 (22.4–23.3)
Female 12,764 916.9 13.9 (13.7–14.2)
ART status
Non-ART 7026 148.9 47.2 (46.1–48.3)
ART 15,045 1152.7 12.8 (12.6–13.0)
HIV clinical stage
1 844 180.0 4.7 (4.3–5.0)
2 2306 300.1 7.7 (7.4–8.0)
3 13,233 604.8 21.9 (21.5–22.2)
4 5214 216.7 24.1 (23.4–24.7)
Age group (years)
< 15 2034 97.5 20.8 (20.0–21.8)
15–24 1210 70.4 17.2 (16.3–18.2)
25–34 5514 323.1 16.9 (16.4–17.3)
35–44 7554 458.9 16.5 (16.1–16.8)
45–54 3990 253.9 15.7 (15.3–16.2)
55+ 1754 116.9 15.0 (14.3–15.7)
TYPICAL TB PRESENTATION IN HIV-POSITIVE
PATIENTS
TB related Condition % of PLHIV who
Develop Condition
Pulmonary disease 75%
Hilar/ mediastinal adenopathy 20 - 59 %
Pleural effusions 12 - 28 %
Miliary pattern 7 - 18 %
Normal CXR, positive sputum
culture
12 %
TUBERCULOSIS-HUMAN IMMUNODEFICIENCY
VIRUS (HIV) CO-INFECTION IN ETHIOPIA: A
SYSTEMATIC REVIEW AND META-ANALYSIS
TEWELDEMEDHIN ET AL. BMC INFECTIOUS DISEASES (2018) 18:676
Our searches returned a total of (n = 26,746) records from 30
articles of which 21 were cross-sectional,
7 were retrospectives and 2 were prospective studies. The
range of prevalence of TB-HIV co-infection was found to
be from 6 to 52.1% with random effects pooled prevalence of
22% (95% CI 19–24%) and with substantial
heterogeneity chi-square (X2) = 746.0, p < 0.001, (I2 =
95.84%).
EFFECT OF TUBERCULOSIS INFECTION ON MORTALITY OF
HIV-INFECTED PATIENTS IN NORTHERN TANZANIA. MOLLEL
ET AL. TROPICAL MEDICINE AND HEALTH (2020) 48:26
The overall mortality rate of 28.4 (95% CI 27.6–29.2)
per 1000 person years.
The mortality rate was 26.2 (95% CI 25.4–27.0)
per 1000 person-years among PLHIV who had no TB,
and 57.8 (95% CI 53.6–62.3) per 1000 person-years
among those with HIV/TB co-infection .
ISONIAZID PREVENTIVE THERAPY PLUS ANTIRETROVIRAL
THERAPY FOR THE PREVENTION OF TUBERCULOSIS: A
SYSTEMATIC REVIEW AND META-ANALYSIS OF INDIVIDUAL
PARTICIPANT DATA
JENNIPHER M ROSS ET AL 2021
 Risk for tuberculosis was lower in participants given
isoniazid preventive therapy and ART than participants given
ART alone (hazard ratio [HR] 0·68, 95% CI 0·49-0·95,
p=0·02). Risk of all-cause mortality was lower in participants
given isoniazid preventive therapy and ART than participants
given ART alone, but this difference was non-significant (HR
0·69, 95% CI 0·43-1·10, p=0·12).
IMPACT OF ISONIAZID PREVENTIVE THERAPY ON TUBERCULOSIS
INCIDENCE AMONG PEOPLE LIVING WITH HIV: A SECONDARY DATA
ANALYSIS USING INVERSE PROBABILITY WEIGHTING OF INDIVIDUALS
ATTENDING HIV CARE AND TREATMENT CLINICS IN TANZANIA
Werner M. Maokola et all 2021
 PLHIV enrolled in 315 HIV care and treatment clinic 2012-2016
Results
 Of 171,743 PLHIV enrolled in the clinics over the five years, 10,326
(6.01%) were excluded leaving 161,417 available for the analysis. Of
the 24,800 who received IPT, 1.00% developed TB disease
whereas of the 136,617 who never received IPT 6,085 (4.98%)
developed TB disease. In 278,545.90 person-years of follow up, a
total 7,052 new TB cases were diagnosed. Using the weighted
sample, the overall TB incidence was 11.57 (95% CI: 11.09–12.07)
per 1,000 person-years. The TB incidence among PLHIV who
received IPT was 10.49 (95% CI: 9.11–12.15) per 1,000 person-
years and 12.00 (95% CI: 11.69–12.33) per 1,000 person-years in
those who never received IPT. After adjusting for other covariates
there was 52% lower risk of developing TB disease among those
who received IPT compared to those who never received IPT: aHR =
0.48 (95% CI: 0.40–0.58, P<0.001)
OPPORTUNISTIC INFECTIONS
TREATMENT WITH ARTS
 Types of Antiretroviral Drugs
1.The recommended antiretroviral drugs to be used in Tanzania
guidelines fall into the following five main categories:
1.Nucleotide reverse transcriptase inhibitors (NtRTIs)
2. Nucleoside reverse transcriptase inhibitors (NRTIs)
3.Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
4. Protease inhibitors (Pls)
5. Integrase strand transfer inhibitors (INSTI)/ Integrase
inhibitors
 Other antiretroviral drugs used elsewhere include:
5.Fusion inhibitors e.g. Enfuvirtide (ENF)
6.Chemokine receptor inhibitors/ CCR5 inhibitors e.g. Maraviroc
TREATMENT WITH ARTS
A.Nucleotide Reverse Transcriptase Inhibitors (NtRTIs)Eg.
1.Tenofovir disoproxil fumarate (TDF)
2.Tenofovir alafenamide (TAF)
B. Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
1.Zidovudine (AZT)
2.Lamivudine (3TC)
3.Emtricitabine (FTC)
4.Abacavir (ABC)
C. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs
 1st generation NNRTIs
1.Nevirapine (NVP) 2. Efavirenz (EFV)
2nd generation NNRTIs
1.Etravirine (ETR )
TREATMENT WITH ARTS CONT………
 Protease Inhibitors (PIs)
 1st generation currently available Protease Inhibitors (PIs)
1.Atazanavir (ATV).
2.Lopinavir (LPV),
3.Ritonavir (usually used as a booster with other PIs)
2nd generation currently available Protease Inhibitors (PIs)
Darunavir (DRV)
Integrase Strand Transfer Inhibitors (INSTI)/ Integrase
inhibitors
1.Dolutegravir (DTG) 2.Raltegravir
(RAL)
TREATMENT WITH ART
FIRST LINE REGIMEN USED IN TANZANIA
ART Initiation: within 7 days of a positive HIV test, unless
there is a medical or psychosocial contraindication
a) DTG based regimens:
TDF + 3TC + DTG (Default first Line regimen)
o ABC + 3TC+ DTG
 AZT+ 3TC+ DTG
 b) EFV based regimens:
 TDF + 3TC + EFV600 or EFV400 TDF+FTC+EFV600
or EFV400
c) NVP based regimens:
 AZT+3TC+NVP
2ND LINE
 Adults, adolescents (>15 years) and Pregnant women /
breastfeeding mothers
AZT/3TC+ATV/r: if TDF was used in first-line
 TDF/FTC+ATV/r: if AZT was used in first line
 Who Inject Drugs (PWID) AZT/3TC + DTG
3RD LINE
Adults, adolescents (>15 years)
DTG+DRV/r+AZT/3TC
People Who Inject Drugs (PWID)
DTG+DRV/r+AZT/3TC
HIV and TB co-infection
DTG (BD) + LPV/r+ (AZT/3TC or
TDF/FTC)
THE IMPACT OF ANTIRETROVIRAL THERAPY ON ADULT
MORTALITY IN RURAL TANZANIA MILLY MARSTON1, DENNA MICHAEL2, WRINGE1, RAPHAEL
ISINGO2, BENJAMIN D. CLARK1,2, ASWILE JONAS2,JULIUS MNGARA2, SAMWELI KALONGOJI2, JOYCE MBAGA3, JOHN CHANGALUCHA2, JIM TODD1,
BASIA ZABA1 AND MARK URASSA AUGUST 2012
 Results
 Overall, the crude adult mortality rate among 15–59-year
olds declined by 17% (hazard rate ratio (HRR) = 0.83;
95%CI: 0.72–0.95) between the pre-ART and the post-ART
periods. This change in mortality over the two time periods was
predominantly because of a fall in female mortality from 8.8
deaths per 1000 person-years to 6.5 deaths per 1000
person-years (HRR = 0.73; 95%CI: 0.60–0.89). The crude
male mortality rate remained similar over the two time periods
at 9.1 in the pre-ART period and 8.5 in the post-ART period.
Over the whole time period, the crude mortality rate in those
who are HIV positive is very high compared with those who are
HIV negative, with a hazard rate ratio of 11.4 (95% CI: 8.9–4.7)
for men and 9.4 (95% CI: 7.4–12.12) for women.
IMMUNE RECONSTITUTION
INFLAMMATORYSYNDROME(IRIS)
 A spectrum of clinical signs and symptoms
resulting from the body’s restored ability to
mount an inflammatory response associated
with immune recovery
 Worsening of symptoms of OI’s that were
already under effective treatment (TB,)
shortly after starting ART
 May be confused with new infection.
 Difficult to distinguish with: side effects,
relapse, treatment resistance
PATHOGENESIS OF IRIS:
 The likelihood and severity of IRIS correlates with
two interrelated factors:
 The extent of CD4 T-cell immune suppression prior
to initiation of ART
 The degree of viral suppression and immune
recovery following initiation of ART
CLINICAL PRESENTATION
General features include:
 Fever
 Worsening of inflammatory response to infection or
antigen
MANAGEMENT PRINCIPLES:
 Consider other possible etiologies
 Continue ART if possible (interrupt if life
threatening)
 Attempt to diagnose infection or condition
responsible for IRIS
 Initiate disease specific therapy if not in place
 Provide anti-inflammatory therapy
HIV RESISTANCE
 The mainstay of resistance of HIV is Mutations.
1. High replication rate: they produce billions of
virions per day account for rapid emergence of viral
variants
2. Lack of proofreading activity of reverse
transcriptase and recombination
PREVALENCE OF REVERSE TRANSCRIPTASE AND PROTEASE
MUTATIONS ASSOCIATED WITHANTIRETROVIRAL DRUG RESISTANCE
AMONG DRUG-NAÏVEHIV-1 INFECTED PREGNANT WOMEN IN KAGERA
AND KILIMANJARO REGIONS,
TANZANIA
BALTHAZAR M NYOMBI ET AL 21 JUNE 2008
 Methods: 100 HIV-1 pregnant women of 246.
 Results:HIV-1 subtypes A, C, D, CRF10_CD and Unique
Recombinant Forms (URF) were detected. Primary mutations
associated with NRTI and NNRTI resistance were detected
among 3% and 4% of treatment-naïve strains, Primary
mutations associated with NRTI and NNRTI resistance were
detected in 1.6% and 11.5% of women who had received sd
NVP, respectively. None of the primary mutations associated
with PI resistance was found.
CONTROL OF DRUG RESISTANCE
 Adherence
 Use of multidrug therapy
 Determine HIV status before administering PEP
 Genotypic resistance surveillance

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  • 1. HIV/ AIDS DR.HAMISI MKINDI,MD. TO DOWNLOAD CONTACT: hermyc@live.com
  • 2. OBJECTIVES 1.Introduction 2.Virology & Immunology 3.Natural history of HIV 4.Pathogenesis and Transmission 5.Lab Testing and Algorithm 6.Hiv & Tb 7..Oi’s 8.Art 9.Iris 910Art Resistance And Treatment Failure 11..Prevention
  • 3. INTRODUCTION  AIDS means Acquired Immunodeficiency Syndrome  HIV means Human immunodeffiency virus HIV is the virus that causes immune deficiency  AIDS is the progression of HIV infection due to destruction of immune system leading to occurrence of diseases.
  • 4. HIV  HIV:Human Immunodeficiency Virus  HIV is the virus that can ultimately lead to AIDS  HIV like other viruses needs to enter other cells in order to replicate.
  • 5. NATURAL HISTORY OF HIV INFECTION
  • 6. VIROLOGY & IMMUNOLOGY:  HIV is a single stranded RNA retrovirus from the Lentivirus family.  It consists of a cylindrical center surrounded by a sphere shaped lipid envelope. The center consists of 1 single strand with two molecules of RNA.  The virus can use RNA & host’s DNA to make viral DNA.
  • 7.
  • 8. VIRAL GENES: NAME OF GENE FUNCTIONS LTR The Long Terminal Repeats are used for integration of the virus into the host genome and also contain promoter and enhancer sequences. gag The Group-specific Antigen corresponds to the core and capsid proteins. pol: This gene encodes the reverse transcriptase, which actually has several functions env: This Envelope gene encodes the gp120 glycoprotein. tat/rev This region encodes factors involved in transactivation and other regulatory functions.
  • 9. RETROVIRAL STRUCTURAL GENES  gag = group specific antigen (internal structural proteins) matrix (MA), binds envelope, organization capsid (CA), protects genome and enzymes nucleocapsid (NC) chaperones RNA, buds  pol = polymerase enzymes reverse transcriptase + RNA to DNA RNAase H (RT) degrades template RNA protease (PR) maturation of precursors integrase (IN) provirus integration  env = envelope proteins surface glycoprotein (SU) receptor binding transmembrane protein (TM) virus-cell fusion
  • 10.
  • 11. CLASSIFICATION:  Types  HIV-1  HIV-2  HIV-1 Groups Subtypes Recombinants Major (M) A,B,C,D,E,F,G,H,I,J AG,AE,AB,CRFs Outlier (O) Novel (N)  HIV-2: 6 subtypes, A,B,C,D,E,F  Jawetz Melnick and Adelberg. Medical Microbiology AIDS and Lentiviruses Mc Graw- Education chpt 44 fourth ed 2007
  • 12. MAJOR STEPS IN HIV LIFECYCLE 1. The virus attaches itself to CD4+ T lymphocytes 2. Fusion and release of RNA into the cytoplasm 3. Reverse transcription to produce pro-viral DNA 4. Integration of pro-viral DNA within host DNA and synthesis of viral proteins 5. Viral assembly and release of mature particles
  • 13. LIFE CYCLE AND DRUGS Warren Levinston review of medical microbiology and immunology, pathogenesis and immunology Mc Graw-Education ed 13 pg 825 2014
  • 14. IMMUNE SYSTEM/BODY DEFENCE  Host defenses against viruses fall into two major categories; 1.Nonspecific defenses;- interferons, natural killer cells 2.Specifc defence ;-humoral, cell-mediated immunity  NONSPECIFIC DEFENSES Alpha and beta interferons are a proteins produced by human cells after viral infection (or after exposure to other inducers They block the synthesis of viral proteins.
  • 15. MECHANISM OF ON HOW THEY ACT  One is a ribonuclease that degrades mRNA  The other is a protein kinase that inhibits protein synthesis.  Interferons are divided into three groups based on the cell of origin, namely, leukocyte, fibroblast, and lymphocyte, They are also known as alpha, beta, and gamma interferons, respectively  Alpha and beta interferons are induced by viruses
  • 16. PATHOGENESIS OF HIV INFECTION HIV infection leads to profound pathology, either directly, through destruction of CD4+ T cells, other immune cells, and neuroglial cells, or indirectly, through the secondary effects of CD4+ T-cell dysfunction and resultant immunosuppression. Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood,
  • 17. 1.HUMAN IMMUNODEFICIENCY VIRUS -MEDIATED INHIBITION OF HEMATOPOIESIS.- -failure of normal hematopoiesis is an obvious candidate mechanism to account for depletion of CD4+T cells during HIV infection
  • 18. 2.AUTOIMMUNITY-molecular mimicry between HIV-1 envelope constituents and host proteins lead to pathogenic autoimmunity → cell death.
  • 19. 3.INNOCENT BYSTANDERS. Uninfected cells may die in an innocent bystander scenario: HIV particles may bind to the cell surface, giving them the appearance of an infected cell and marking them for destruction by killer T cells (cellular immune response).
  • 20. 4.SYNCYTIA FORMATION. Infected cells also may fuse with nearby uninfected cells through CD4-mediated fusion, forming balloon (multinucleared)-like giant cells called syncytia. This mechanism of cell-to-cell spread of HIV has been associated with the death of uninfected cells. The presence of syncytia-inducing variants of HIV has been correlated with rapid disease progression in HIV-infected individuals.
  • 21. PATHOGENESIS CONT….. 5.APOPTOSIS and Pyoptosis. Infected CD4+ T cells may be killed when cellular regulation is distorted by HIV proteins, probably leading to their suicide by a process known as programmed cell death or apoptosis mediated by caspase3. -Uninfected cells also may undergo apoptosis. -Investigators have shown in cell cultures that the HIV envelope alone or bound to antibodies sends an inappropriate signal to CD8+ T cells causing them to undergo apoptosis even though not infected by HIV.
  • 22. PYROPTOSIS  It has been known for some time now that apoptosis is a major factor contributing to T-cell depletion, mediated by caspase-3, in T-cells that are permissive to infection by HIV. However, there are subsets of T-cells (abortive T-cells) that are non-permissive and do not support HIV replication. In this subset of cells, cell death occurs through a process called pyroptosis, driven by caspase-1  Pyroptosis is a highly inflammatory form of programmed cell death in which the dying cell releases all its cytoplasmic contents, including inflammatory cytokines; these cytokines in turn trigger pyroptosis in other T-cells as part of a vicious cycle of abortive T- cell depletion
  • 23. 6.DIRECT CELL KILLING. Infected CD4+ T cells may be killed directly when large amounts of virus are produced and bud off from the cell surface, disrupting the cell membrane, or when viral proteins(gp120) and nucleic acids collect inside the cell, interfering with cellular machinery → cell death.
  • 24.  Regulatory T-Cells (Treg)  Chronic immune Activation  immune Activation and inflammation -Cytikine storm,il 2 inhibited hence no maturation of t cells
  • 25. RISK FACTORS FOR HIV IN THE GENERAL POPULATION TRANSMISSION 1.MEN WHO HAVE SEX WITH MEN Study done in Dar es Salaam, Tanzania by Nyoni and Ross in 2013 found that condom usage was very low among the MSM, another study in Zanzibar 85% of the respondents reported inconsistent condom use(M. Dahoma, L. et al 2011.Prevalence (22-42%) (Leshabari et al. A Prevalence of the Human Immunodeficiency Virus, other sexually transmitted infections, and health-related perceptions, reflections, experiences and practices among men having sex with men in Dar 2013) 2.FEMALE SEX WORKERS mobile populations and sex workers Prevalence 14-35%)(National AIDS Control Programme; A study of Female Sex Workers in seven Regions: Dar es Salaam, Iringa, Mbeya, Mwanza, Shinyanga, Tabora and Mara. A Report published in 2014 (ISBN 978-9987-650-83-5)
  • 26. RISK FACTORS FOR HIV IN THE GENERAL POPULATION CONT….. 3.PEOPLE WHO INJECT DRUGS (PWID). PWID and their partners represent another population that can serveas a “bridging population” for HIV transmission. prevalence 16-51%(Dar es salaam. Integrated Bio-Behavioural Survey Among People Who Inject Drugs in Dar es Salaam. April 16, 2014) 4.MOBILE POPULATION like,fishermen, prisoners and truck drivers (Anthony Kapesa1 et al 2018) bridging population.
  • 27. RISK FACTORS FOR HIV IN THE GENERAL POPULATION CONT…..  The prevalence of HIV among young people aged 15- 19 years was 1% (1.3% among girls, and 0.8% among boys). Furthermore, the percentage of women aged 20-24 infected with HIV is higher (4.4%) than that of men (1.7%) in the same age group.(National Bureau of Statistics, ICF International. Tanzania HIV AND AIDS and Malaria Indicator Survey 2011-12. Dar es Salaam, March 2013).  Women are disproportionally more affected, with an HIV prevalence of 6.3 % versus 3.9% among men. (THMIS 2011-12).
  • 28. PREVENTION OF HIV INFECTION 1.MOTHER-TO-CHILD TRANSMISSION OF HIV( PMTCT) during, labour, delivery or breastfeeding ranges from 15% to 45%. PMTCT) interventions can reduce this risk to below 5% (World Health Organization (WHO) 'Mother-to-child transmission of HIV' [accessed November 2018])
  • 29. 2.PRE EXPOSURE PROPHYLAXIS (PREP) POST EXPOSURE PROPHYLAXIS (PEP)  PrEP. Prevent by 70%(Virginia A Fonner et al 2016 Jul.)  Populations targeted for PrEP include Sex workers, Men who have sex with men, People who inject drugs, Vulnerable adolescent girls (15-19) and Young women (20-24) and Sero- discordant couples. The recommended PrEP regimen in Tanzania is: Emtricitabine (FTC) 200 mg/Tenofovir Disoproxil Fumarate (TDF) 300 mg (Truvada) PO Daily. PEP.The guidelines recommend the use of TLD (TDF+3TC/FTC+DTG) for adults and adolescents
  • 30. 3.VOLUNTARY MEDICAL MALE CIRCUMCISION (VMMC) reduces female-to-male sexual transmission of HIV by 60%.(Auvert, B et al. (2005) In Tanzania, the national prevalence of male circumcision 77.6% among male aged 15 years and older (THIS 16/17)
  • 32.
  • 33. LABORATORY DIAGNOSTICS IN HIV INFECTION Antibody detection using rapid tests/ELISA Virological tests Assays to detect p24 antigen Assays to detect HIV DNA or RNA (PCR) Viral culture
  • 34. LABORATORY DIAGNOSTICS IN HIV INFECTION CONT........................ Antibody methods for diagnosing HIV include:  Rapid tests  Enzyme Linked Immunosorbent Assay (ELISA)  Western Blot (confirmatory test if available) Effective 12 weeks after infection, as antibodies appear 6 to 12 weeks following HIV infection in a majority of patients Not suitable for use in infants under 18 months (use PCR)
  • 35. LABORATORY DIAGNOSTICS IN HIV INFECTION CONT..... p24 tests Detect the p24 antigen. Based on the detection of antibodies against HIV-1 antigens in serum. Can be effective 2 to 3 weeks after HIV infection. Detect HIV antigen before antibody can be detected.
  • 36. LABORATORY DIAGNOSTICS IN HIV INFECTION CONT........ DNA PCR tests Useful in early diagnosis and infant diagnosis (<18 months)
  • 37. TB/HIV CO-INFECTION Tuberculosis (TB) is a disease caused by a bacterium called Mycobacterium tuberculosis. TB is spread by airborne route: droplet nuclei When a person with TB disease of the lungs coughs or speaks, droplets of TB bacteria spread through the air. Once in the body, TB can be inactive or
  • 38. THE IMAGE BELOW SHOWS THE DIFFERENCE BETWEEN LATENT TB INFECTION AND TB DISEASE
  • 39. TB/HIV CO-INFECTION CONT...... When the TB bacterium is inactive, this is called Latent TB infection. When the TB bacterium is active, this is called TB disease. Most exposed people do not become infected. Persons co-infected with HIV and TB have highest risk for developing TB disease
  • 40. TB/HIV CO-INFECTION CONT......  The lifetime risk of developing activeTB among people living with HIV (PLHIV) maybe 20 times higher than in people without HIV [Organization WH. Global report TB 2015].  Tanzania is among the 30 countries with high TB burden and TB and HIV co-infection in the world. [Organization WH. Global tuberculosis report 2018]  Despite the increased access to antiretroviral therapy (ART), mortality in PLHIV is still high, and TB is the leading cause of mortality[Lawn SD,et al 2008]’  Some studies found that TBpreventive therapy by isoniazid reduces the incidence of TB in HIV-infected Patients.(Mwinga A et all 1999)
  • 41. TB/HIV CO-INFECTION CONT......  Impact of HIV on TB:  HIV is a high risk factor for the development of TB  HIV increases risk of recurrent TB  HIV promotes progression to active TB in people with both recently acquired and latent M. tuberculosis  Impact of TB on HIV:  TB is the leading cause of death among PLHIV  TB increases the risk of progression from HIV to AIDS  TB is the most common OI in HIV infected people
  • 42. TB/HIV CO-INFECTION CONT...... Clinical presentation Atypical presentation of pulmonary disease Extra-pulmonary manifestations Diagnosis of TB More smear negative (low bacterial load) HIV positive persons are more likely to have a negative TB skin test due to skin test anergy (especially if CD4 is low)
  • 43. Characteristics 2011 2012 2013 2014 Total Overall 8765 (2.1) 9798 (2.3) 11,212 (2.5) 9857 (1.9) 39,632 (2.2) Age group < 15 years 687 (2.1) 784 (2.3) 1066 (3.2) 854 (2.4) 3391 (2.5) ≥ 15 years 8078 (2.1) 9014 (2.3) 10,146 (2.4) 9003 (1.9) 36,241 (2.2) Sex Male 3858 (2.9) 4474 (3.2) 5066 (3.5) 4681 (2.8) 18,079 (3.1) Female 4907 (1.8) 5324 (1.8) 6146 (2.0) 5176 (1.5) 21,553 (1.7) ART status ART 1145 (1.5) 883 (1.4) 630 (1.2) 699 (1.2) 3357 (1.3) Non-ART 7620 (2.3) 8915 (2.4) 10,582 (2.6) 9158 36,275 (2.3) Table 2 Prevalence of TB among individuals enrolled in HIV care, treatment, and support program in Tanzania from 2011 to 2014. . Majigo et al. 2020
  • 44. Variable TB cases 1000 person-years TB incident rate Overall 22,071 1323.6 16.7 (16.4–16.9) Year of diagnosis 2011 5366 316.2 17.0 (16.5–17.4) 2012 5254 317.9 16.5 (16.1–17.0) 2013 6356 348.5 18.2 (17.8–18.7) 2014 5095 342.3 14.9 (14.5–15.4) Sex Male 9306 407.7 22.8 (22.4–23.3) Female 12,764 916.9 13.9 (13.7–14.2) ART status Non-ART 7026 148.9 47.2 (46.1–48.3) ART 15,045 1152.7 12.8 (12.6–13.0) HIV clinical stage 1 844 180.0 4.7 (4.3–5.0) 2 2306 300.1 7.7 (7.4–8.0) 3 13,233 604.8 21.9 (21.5–22.2) 4 5214 216.7 24.1 (23.4–24.7) Age group (years) < 15 2034 97.5 20.8 (20.0–21.8) 15–24 1210 70.4 17.2 (16.3–18.2) 25–34 5514 323.1 16.9 (16.4–17.3) 35–44 7554 458.9 16.5 (16.1–16.8) 45–54 3990 253.9 15.7 (15.3–16.2) 55+ 1754 116.9 15.0 (14.3–15.7)
  • 45. TYPICAL TB PRESENTATION IN HIV-POSITIVE PATIENTS TB related Condition % of PLHIV who Develop Condition Pulmonary disease 75% Hilar/ mediastinal adenopathy 20 - 59 % Pleural effusions 12 - 28 % Miliary pattern 7 - 18 % Normal CXR, positive sputum culture 12 %
  • 46. TUBERCULOSIS-HUMAN IMMUNODEFICIENCY VIRUS (HIV) CO-INFECTION IN ETHIOPIA: A SYSTEMATIC REVIEW AND META-ANALYSIS TEWELDEMEDHIN ET AL. BMC INFECTIOUS DISEASES (2018) 18:676 Our searches returned a total of (n = 26,746) records from 30 articles of which 21 were cross-sectional, 7 were retrospectives and 2 were prospective studies. The range of prevalence of TB-HIV co-infection was found to be from 6 to 52.1% with random effects pooled prevalence of 22% (95% CI 19–24%) and with substantial heterogeneity chi-square (X2) = 746.0, p < 0.001, (I2 = 95.84%).
  • 47. EFFECT OF TUBERCULOSIS INFECTION ON MORTALITY OF HIV-INFECTED PATIENTS IN NORTHERN TANZANIA. MOLLEL ET AL. TROPICAL MEDICINE AND HEALTH (2020) 48:26 The overall mortality rate of 28.4 (95% CI 27.6–29.2) per 1000 person years. The mortality rate was 26.2 (95% CI 25.4–27.0) per 1000 person-years among PLHIV who had no TB, and 57.8 (95% CI 53.6–62.3) per 1000 person-years among those with HIV/TB co-infection .
  • 48. ISONIAZID PREVENTIVE THERAPY PLUS ANTIRETROVIRAL THERAPY FOR THE PREVENTION OF TUBERCULOSIS: A SYSTEMATIC REVIEW AND META-ANALYSIS OF INDIVIDUAL PARTICIPANT DATA JENNIPHER M ROSS ET AL 2021  Risk for tuberculosis was lower in participants given isoniazid preventive therapy and ART than participants given ART alone (hazard ratio [HR] 0·68, 95% CI 0·49-0·95, p=0·02). Risk of all-cause mortality was lower in participants given isoniazid preventive therapy and ART than participants given ART alone, but this difference was non-significant (HR 0·69, 95% CI 0·43-1·10, p=0·12).
  • 49. IMPACT OF ISONIAZID PREVENTIVE THERAPY ON TUBERCULOSIS INCIDENCE AMONG PEOPLE LIVING WITH HIV: A SECONDARY DATA ANALYSIS USING INVERSE PROBABILITY WEIGHTING OF INDIVIDUALS ATTENDING HIV CARE AND TREATMENT CLINICS IN TANZANIA Werner M. Maokola et all 2021  PLHIV enrolled in 315 HIV care and treatment clinic 2012-2016 Results  Of 171,743 PLHIV enrolled in the clinics over the five years, 10,326 (6.01%) were excluded leaving 161,417 available for the analysis. Of the 24,800 who received IPT, 1.00% developed TB disease whereas of the 136,617 who never received IPT 6,085 (4.98%) developed TB disease. In 278,545.90 person-years of follow up, a total 7,052 new TB cases were diagnosed. Using the weighted sample, the overall TB incidence was 11.57 (95% CI: 11.09–12.07) per 1,000 person-years. The TB incidence among PLHIV who received IPT was 10.49 (95% CI: 9.11–12.15) per 1,000 person- years and 12.00 (95% CI: 11.69–12.33) per 1,000 person-years in those who never received IPT. After adjusting for other covariates there was 52% lower risk of developing TB disease among those who received IPT compared to those who never received IPT: aHR = 0.48 (95% CI: 0.40–0.58, P<0.001)
  • 51. TREATMENT WITH ARTS  Types of Antiretroviral Drugs 1.The recommended antiretroviral drugs to be used in Tanzania guidelines fall into the following five main categories: 1.Nucleotide reverse transcriptase inhibitors (NtRTIs) 2. Nucleoside reverse transcriptase inhibitors (NRTIs) 3.Non-nucleoside reverse transcriptase inhibitors (NNRTIs) 4. Protease inhibitors (Pls) 5. Integrase strand transfer inhibitors (INSTI)/ Integrase inhibitors  Other antiretroviral drugs used elsewhere include: 5.Fusion inhibitors e.g. Enfuvirtide (ENF) 6.Chemokine receptor inhibitors/ CCR5 inhibitors e.g. Maraviroc
  • 52. TREATMENT WITH ARTS A.Nucleotide Reverse Transcriptase Inhibitors (NtRTIs)Eg. 1.Tenofovir disoproxil fumarate (TDF) 2.Tenofovir alafenamide (TAF) B. Nucleoside Reverse Transcriptase Inhibitors (NRTIs) 1.Zidovudine (AZT) 2.Lamivudine (3TC) 3.Emtricitabine (FTC) 4.Abacavir (ABC) C. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs  1st generation NNRTIs 1.Nevirapine (NVP) 2. Efavirenz (EFV) 2nd generation NNRTIs 1.Etravirine (ETR )
  • 53. TREATMENT WITH ARTS CONT………  Protease Inhibitors (PIs)  1st generation currently available Protease Inhibitors (PIs) 1.Atazanavir (ATV). 2.Lopinavir (LPV), 3.Ritonavir (usually used as a booster with other PIs) 2nd generation currently available Protease Inhibitors (PIs) Darunavir (DRV) Integrase Strand Transfer Inhibitors (INSTI)/ Integrase inhibitors 1.Dolutegravir (DTG) 2.Raltegravir (RAL)
  • 55. FIRST LINE REGIMEN USED IN TANZANIA ART Initiation: within 7 days of a positive HIV test, unless there is a medical or psychosocial contraindication a) DTG based regimens: TDF + 3TC + DTG (Default first Line regimen) o ABC + 3TC+ DTG  AZT+ 3TC+ DTG  b) EFV based regimens:  TDF + 3TC + EFV600 or EFV400 TDF+FTC+EFV600 or EFV400 c) NVP based regimens:  AZT+3TC+NVP
  • 56. 2ND LINE  Adults, adolescents (>15 years) and Pregnant women / breastfeeding mothers AZT/3TC+ATV/r: if TDF was used in first-line  TDF/FTC+ATV/r: if AZT was used in first line  Who Inject Drugs (PWID) AZT/3TC + DTG
  • 57. 3RD LINE Adults, adolescents (>15 years) DTG+DRV/r+AZT/3TC People Who Inject Drugs (PWID) DTG+DRV/r+AZT/3TC HIV and TB co-infection DTG (BD) + LPV/r+ (AZT/3TC or TDF/FTC)
  • 58.
  • 59. THE IMPACT OF ANTIRETROVIRAL THERAPY ON ADULT MORTALITY IN RURAL TANZANIA MILLY MARSTON1, DENNA MICHAEL2, WRINGE1, RAPHAEL ISINGO2, BENJAMIN D. CLARK1,2, ASWILE JONAS2,JULIUS MNGARA2, SAMWELI KALONGOJI2, JOYCE MBAGA3, JOHN CHANGALUCHA2, JIM TODD1, BASIA ZABA1 AND MARK URASSA AUGUST 2012  Results  Overall, the crude adult mortality rate among 15–59-year olds declined by 17% (hazard rate ratio (HRR) = 0.83; 95%CI: 0.72–0.95) between the pre-ART and the post-ART periods. This change in mortality over the two time periods was predominantly because of a fall in female mortality from 8.8 deaths per 1000 person-years to 6.5 deaths per 1000 person-years (HRR = 0.73; 95%CI: 0.60–0.89). The crude male mortality rate remained similar over the two time periods at 9.1 in the pre-ART period and 8.5 in the post-ART period. Over the whole time period, the crude mortality rate in those who are HIV positive is very high compared with those who are HIV negative, with a hazard rate ratio of 11.4 (95% CI: 8.9–4.7) for men and 9.4 (95% CI: 7.4–12.12) for women.
  • 60. IMMUNE RECONSTITUTION INFLAMMATORYSYNDROME(IRIS)  A spectrum of clinical signs and symptoms resulting from the body’s restored ability to mount an inflammatory response associated with immune recovery  Worsening of symptoms of OI’s that were already under effective treatment (TB,) shortly after starting ART  May be confused with new infection.  Difficult to distinguish with: side effects, relapse, treatment resistance
  • 61. PATHOGENESIS OF IRIS:  The likelihood and severity of IRIS correlates with two interrelated factors:  The extent of CD4 T-cell immune suppression prior to initiation of ART  The degree of viral suppression and immune recovery following initiation of ART
  • 62. CLINICAL PRESENTATION General features include:  Fever  Worsening of inflammatory response to infection or antigen
  • 63. MANAGEMENT PRINCIPLES:  Consider other possible etiologies  Continue ART if possible (interrupt if life threatening)  Attempt to diagnose infection or condition responsible for IRIS  Initiate disease specific therapy if not in place  Provide anti-inflammatory therapy
  • 64. HIV RESISTANCE  The mainstay of resistance of HIV is Mutations. 1. High replication rate: they produce billions of virions per day account for rapid emergence of viral variants 2. Lack of proofreading activity of reverse transcriptase and recombination
  • 65. PREVALENCE OF REVERSE TRANSCRIPTASE AND PROTEASE MUTATIONS ASSOCIATED WITHANTIRETROVIRAL DRUG RESISTANCE AMONG DRUG-NAÏVEHIV-1 INFECTED PREGNANT WOMEN IN KAGERA AND KILIMANJARO REGIONS, TANZANIA BALTHAZAR M NYOMBI ET AL 21 JUNE 2008  Methods: 100 HIV-1 pregnant women of 246.  Results:HIV-1 subtypes A, C, D, CRF10_CD and Unique Recombinant Forms (URF) were detected. Primary mutations associated with NRTI and NNRTI resistance were detected among 3% and 4% of treatment-naïve strains, Primary mutations associated with NRTI and NNRTI resistance were detected in 1.6% and 11.5% of women who had received sd NVP, respectively. None of the primary mutations associated with PI resistance was found.
  • 66. CONTROL OF DRUG RESISTANCE  Adherence  Use of multidrug therapy  Determine HIV status before administering PEP  Genotypic resistance surveillance