Presented by Dr Abdel Hady Mesbah at the Egyptian African Critical Care Summit. The Summit was organized by Scribe

1. TOWARDS A WORLD
WITHOUTAIDS
By : Dr. Abdelhady M. Elmahdy M.D.
Fellow Of The AmericanAcademy Of Immunology
E-mail : Hadymesbah@yahoo.Com

2. HISTORY OF HIV
1930
HIV-1
arises
1959
Earliest
sero-positive
1981
AIDS
emerges
1983
HIV-1
identified
1986
HIV-2
identified
1997
Advent of
HAART
HIV
2006

3. Transmembrane
glycoprotein (gp41)
Host cell
protein
Lipid layer
Nucleocapsid (p17)
Reverse
transcriptase
Ribonucleic
protein (p24)
RNA with
protein
surround
(p7/p9)
Spike of
envelope
glycoprotein
(gp120)
HIV STRUCTURE

7. IntegraseRNA
DNA
Translation
Protease
Processing
Reverse
transcriptase
Transcription
Reverse
transcriptase
inhibitors
Protease
inhibitors
Replication of HIV:
points of therapeutic intervention
Fusion
Inhibitors

15. AIDS-RELATED DEATHS HAVE FALLEN BY 45% SINCETHE PEAK IN
2005.
IN 2015,1.1 MILLION [940 000–1.3 MILLION] PEOPLE DIED FROMAIDS-
RELATED CAUSES WORLDWIDE,COMPARED TO 2 MILLION [1.7 MILLION–2.3
MILLION] IN 2005.
HIV/TUBERCULOSIS TUBERCULOSIS-RELATED DEATHS AMONG
PEOPLE LIVINGWITH HIV HAVE FALLEN BY 32% SINCE 2004.
-TUBERCULOSIS REMAINSTHE LEADING CAUSE OF DEATH AMONG
PEOPLE LIVINGWITH HIV,ACCOUNTING FOR AROUND ONE INTHREE
AIDS-RELATED DEATHS.
- IN 2014,THE PERCENTAGE OF IDENTIFIED HIV-POSITIVETUBERCULOSIS
PATIENTS WHO STARTED OR CONTINUED ON ANTIRETROVIRALTHERAPY
REACHED 77%

16. REGIONAL STATISTICS—2015
Asia and the Pacific
In 2015,there were 5.1 million [4.4 million–5.9 million] people living with HIV
in Asia and the Pacific.
In 2015,there were an estimated 300 000 [240 000–380 000] new HIV
infections in the region.
- New HIV infections declined by 5% between 2010 and 2015.
In Asia and the Pacific,180 000 [150 000–220 000] people died of AIDS-
related causes in 2015.
- Between 2010 and 2015,the number of AIDS-related deaths in the region
decreased by 24%.
Treatment coverage was 41% [35–47%]of all people living with HIV in Asia
and the Pacific.
An estimated 3 million [2.3 million–3.8 million] adults did not have access to
antiretroviral therapy in Asia and the Pacific in 2015.
There were 19 000 [16 000–22 000] new HIV infections among children in
Asia and the Pacific in 2015.
- Since 2010,there has been a 26% decline in new HIV infections among
children in the region.

17. Eastern Europe and centralAsia
In 2015, there were 1.5 million [1.4 million–1.7 million] people
living with HIV in eastern Europe and central Asia.
In 2015, there were an estimated 190 000 [170 000–200 000]
new HIV infections in the region.
- New HIV infections rose by 57% between 2010 and 2015.
In eastern Europe and central Asia, 47 000 [39 000–55 000]
people died of AIDS related causes in 2015.
Between 2010 and 2015,the number of AIDS-related deaths in
the region increased by 22%.
Treatment coverage is 21% [20–23%] of all people living with
HIV in eastern Europe and central Asia.
There were <1000 [<1000–1100] new HIV infections among
children in eastern Europe and central Asia in 2015.

18. East and southern Africa
In 2015,there were 19 million [17.7 million–20.5
million] people living with HIV in eastern and southern
Africa.
- Women account for more than half the total
number of people living with HIV in eastern and
southern Africa.
In 2015,there were an estimated 960 000 [830 000–
1.1 million] new HIV infections in eastern and southern
Africa.
- New HIV infections declined by 14% between 2010
and 2015.
- Eastern and southern Africa accounts for 46% of the
global total of new HIV infections.

19. East and southern Africa(cont.)
In eastern and southern Africa, 470 000 [390 000–560 000] people died of AIDS-related
causes in 2015.
- Between 2010 and 2015,the number of AIDS-related deaths in eastern and
southern Africa fell by 38%.
In eastern and southern Africa, 10.3 million people were accessing antiretroviral
therapy, 54% [50–58%] of all people living with HIV in the region.
- 59% [55–64%] of adult women (aged 15 years and over) and 44% [41–48%] of adult
men were accessing antiretroviral therapy in eastern and southern Africa in 2015.
There were 56 000 [40 000–76 000] new HIV infections among children in eastern
and southern Africa in 2015.
- Since 2010, there has been a 66% decline in new HIV infections among children in
the region

20. Western and central Africa
In 2015, there were 6.5 million [5.3 million–7.8 million]
people living with HIV in western and central Africa.
- Women account for nearly 60% of the total number of
people living with HIV in western and central Africa.
In 2015,there were an estimated 410 000 [310 000–
530 000] new HIV infections in western and central
Africa.
- New HIV infections declined by 8% between 2010 and
2015.
In western and central Africa, 330 000 [250 000–430
000] people died of AIDS-related causes in 2015.
-

21. western and central Africa (cont.)
Between 2010 and 2015, the number of AIDS-
related deaths in western and central Africa fell by
10%.
In western and central Africa, 1.8 million people
were accessing antiretroviral therapy, 28% [23–
34%] of all people living with HIV in the region.
There were 66 000 [47 000–87 000] new HIV
infections among children in western and central
Africa in 2015.
- Since 2010, there has been a 31% decline in new
HIV infections among children in the region.

22. Middle East and North Africa
In 2015, there were 230 000 [160 000–330 000] people living
with HIV in the Middle East and NorthAfrica.
In 2015, there were an estimated 21 000 [12 000–37 000] new
HIV infections in the region.
- New HIV infections rose by 4% between 2010 and 2015.
In the Middle East and North Africa, 12 000 [8700–16 000] people
died of AIDS-related causes in 2015.
- Between 2010 and 2015,the number of AIDS-related deaths in
the region increased by 22%.
Treatment coverage in 2015 was 17% [12–24%] among people
living with HIV in the Middle East and NorthAfrica.
There were 2100 [1400–3200] new HIV infections among
children in the Middle East and NorthAfrica in 2015.

23. •EGYPT
•HIV and AIDS estimates (2015)
• Number of people living with HIV : 11 000 [7200 - 19
000]
•Adults aged 15 to 49 prevalence rate : <0.1% [<0.01%
- <0.1%]
•Women aged 15 and over living with HIV : 3300
[2000 - 5500]
•Children aged 0 to 14 ys living with HIV : <500 [<200
- <500]
•Deaths due to AIDS : <500 [<200 - <1000]
•Orphans due to AIDS aged 0 to 17 : 1900 [1200 -
3300]

24. Latin America and the Caribbean
In 2015, there were 2 million [1.7 million–2.3 million] people living with
HIV in Latin America.
In 2015, there were an estimated 100 000 [86 000–120 000] new HIV
infections in the region.
-The number of new HIV infections did not vary between 2010 and
2015.
In LatinAmerica, 50 000 [41 000–59 000] people died of AIDS-related
causes in 2015.
- Between 2010 and 2015,the number of AIDS-related deaths in the
region fell by 18%.
Treatment coverage in 2015 was 55% [47–64%] among all people
living with HIV in Latin America.
There were 2100 [1600–2900] new HIV infections among children in
Latin America in 2015.

25. Western and central Europe and North America
In 2015,there were 2.4 million [2.2 million–2.7 million] people living
with HIV in western and central Europe and North America.
In 2015,there were an estimated 91 000 [89 000–97 000] new HIV
infections in the region.
In western and central Europe and North America, 22 000 [20
000–24 000] people died of AIDS-related causes in 2015.
- Between 2010 and 2015, the number of AIDS-related deaths in the
region decreased by 24%.

27. •AST/ALT:
•NVP-based ART: 2, 4, and 12 weeks post-initiation,thereafter only as clinically indicated
•EFV-based ART: 4 and 12 weeks post-initiation,thereafter only as clinically indicated
•PI-based ART: only as clinically indicated
•Glucose and total cholesterol/triglycerides annually only if on PI-based
ART
•Creatinine and creatinine clearance : 3 and 6 months post-initiation and
then,if stable,every 6 months (TDF only)
•RPR (rapid plasma reagin )orVDRL test: after baseline,only as indicated

34. •PrEP: Short for “pre-exposure prophylaxis,” PrEP is
an HIV prevention strategy in which HIV-negative
people take an oral pill once a day before coming
into contact with HIV to reduce their risk of HIV
infection. PrEP must be taken for at least 7 days to
reach optimal levels of protection against HIV.
•PEP: Short for “post-exposure prophylaxis,” PEP is
an HIV prevention strategy in which HIV-negative
people take anti-HIV medications after coming into
contact with HIV to reduce their risk of HIV infection.
PEP must be started within 72 hours after HIV
exposure.

35. What is emergency HIV treatment?
Post-exposure prophylaxis, or PEP, is another
name for emergency HIV treatment.
PEP is not a cure for HIV, it is a form of HIV prevention.
It is a short course of antiretroviral drugs that
stops exposure to HIV from becoming a life-long
infection. Taking PEP can cause side effects such as
nausea and fatigue. DO NOT stop taking PEP - talk to
your healthcare professional.
PEP must be taken as soon as possible to be
effective and no later than 72 hours after
exposure to HIV.
PEP must be taken at the same time every day for 4
weeks.

36. Who can get PEP?
Usually you should only take PEP if :
• it has not been longer than 72 hours since exposure
to HIV
● you are not already living with HIV
● a mucous membrane (including: eyes, mouth, vagina,
rectum) has had direct contact with.
● someone’s bodily fluid that might be infectious or an
open wound has had direct contact with someone’s
bodily fluid that might be infectious.
● the source of exposure is infected with HIV or their
HIV status is unknown.2

37. • PEP and HIV testing : It’s normal to feel anxious
about being infected with HIV. Don’t let being
worried stop you from getting an HIV test.
• If you took PEP - get tested 3 and 6 months
after potential exposure.
• If you didn’t take PEP - get tested 3 months
after potential exposure.
• PEP in pregnancy : Certain PEP drugs can be
taken during pregnancy.However,some drugs
should not be used for PEP if you are pregnant.
Speak to a healthcare professional about your
options.

38. HIGHLY ACTIVE ANTIRETROVIRAL
THERAPY (HAART)
 Highly active antiretroviral therapy (HAART) for the chronic
suppression of HIV replication has been the major
accomplishment in HIV/AIDS medicine
 Many patients are now in their second decade of treatment,
with levels of plasma HIV RNA below the limits of detection of
clinical assays
 Many patients are now enjoying a life-style little encumbered
by symptoms or the side effects of medications, many of which
require only once daily administration

39. MAIN OBSTACLE TO HIV CURE
VIRUS LATENCY
The CD4 T cells (T helper cell) and other myeloid, such as bone-marrow-
derived, cells are the main targets of HIV infection. The Problem
is replication-competent HIV provirus can persist in resting CD4 T cells
and maybe in these other cells as well.
Accurately assess latent virus load, is technically difficult to do so
because Methods that measure integrated HIV virus DNA tend
to overestimate latency since they can't discriminate replication-defective
HIV DNA. Similar drawback attends methods that measure HIV RNA. While
the quantitative viral outgrowth assay (QVOA) is far better at measuring
frequency of truly latent, replication-competent provirus, it tends
to underestimate the size of the latent reservoir.

40. WHAT IS THE CURRENT STATE OF THE HIV CURE?
As of 2016, there is one confirmed case of HIV cure, that
of Timothy Ray Brown, one of two of The Berlin Patient. He
was diagnosed with HIV in 1995 while studying in Berlin,
Germany, in 2007 he underwent Hematopoietic stem cell
transplantation from a donor with a rare mutation, which is
homozygous meaning in both alleles. The mutation renders a
person resistant to HIV infection by disabling its entry into
susceptible cells that express CCR5 on their cell surface.
Timothy Ray Brown is considered completely
cured, sterile cure as in no longer harboring HIV in his body. He
is off of antiretroviral therapy (ART).

41. • Two Boston patients were also treated using stem cell
transplantation though not from CCR5-delta32
homozygous donors. However, they experienced relapse
.
• The VISCONTI cohort is a group of 14 French patients who
started ART within the first few weeks of getting HIV infected.
In remission now for 12 years and counting, they're
considered 'functionally' cured of HIV, i.e., continuing to
harbor HIV but no longer needing to take ART.
• The same group's also reported similar outcome for a
perinatally infected case treated from birth for at least
the first 5 years. This patient remained in remission
when re-examined at length at 18 years of age.

42. CLASSIFICATION OF ART DRUGS
• Nucleo(t)side Reverse Transcriptase Inhibitors (NRTIs)
• Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
• Protease Inhibitors (PIs)
• Entry Inhibitors - Chemokine (CCR5) co-receptor antagonist
• Fusion Inhibitors
• Integrase Inhibitors (HIV integrase strand transfer inhibitors)

43. GOALS OFANTIRETROVIRAL
THERAPY
Control of viral replication
Prevention or delay of
progressive
immunodeficiency
Delayed progression to AIDS
Prolonged Survival
Decreased selection of
resistant virus

44. HIV life cycle and antiretroviral drug targets

45. NUCLEO(T)SIDE REVERSE TRANSCRIPTASE
INHIBITORS (NRTIS)
•First agents available for HIV
Infection.
•Less potent than NNRTIs) and
pIs.
•Have a central role in ART.
•Have activity against HIV-1 and
HIV-2.
•Nucleoside and nucleotide analogue
s
•Differ from normal substrates only by
a minor modification in sugar (ribose)
molecule
Drugs
•Abacavir (ABC)
•Didanosine (ddI)
•Emtricitabine (FTC)
•Lamivudine (3TC)
•Stavudine (d4T)
•Tenofovir (TDF)
•Zidovudine (ZDV;
formerly azidothymidine
[AZT])

46. NONNUCLEOSIDE REVERSE TRANSCRIPTASE
INHIBITORS (NNRTIS)
•Were introduced in 1996 with
approval of nevirapine.
•Have potent activity against HIV-1
and are part of preferred initial
regimens.
•Efavirenz, confers most significant
inhibition of viral infectivity
•All exhibit same mechanism of action
Drugs
First-generation
Delavirdine(DLV)
Efavirenz (EFV)
Nevirapine (NVP)
Second-generation
Etravirine (ETR)
Rilpivirine (RPV)

47. PROTEASE INHIBITORS (PIS)
Drugs
• Atazanavir sulfate,ATV
• Darunavir
• Fosamprenavir Calcium,FOS-
APV
• Indinavir,IDV,
• lopinavir / ritonavir, LPV/RTV
• Nelfinavir mesylate,NFV
• Saquinavir mesylate,SQV
• Tipranavir,TPV
• First introduced in
1995
• Are an integral part
of treatment
• Exhibit activity
against clinical
isolates of both HIV-
1 and HIV-2.

48. ENTRY INHIBITORS - CHEMOKINE
(CCR5) CO-RECEPTORANTAGONIST
• Maraviroc
• Binding of gp120 HIV surface protein to CD4 receptor induces a structural
change that revealsV3 loop of the protein.
• V3 loop then binds with a chemokine coreceptor (principally either CCR5 or
CXCR4),allowing gp41 to insert itself into the host cell and leading to fusion of
the cell membranes.
• Maraviroc selectively and reversibly binds CCR5 coreceptor,blockingV3 loop
interaction and inhibiting fusion of cellular membranes.
• As some viral strains may use an alternate co-receptor CXCR4 for entry,
• a tropism assay is necessary to confirm that patient’s virus only uses CCR5 for entry.

49. FUSION INHIBITORS
• Enfuvirtide,
• Act extracellularly to prevent fusion of HIV to CD4 or other target cell.
• Blocks second step in fusion pathway by binding to HR1 region of gp41.
• Does not allow HR1 and HR2 to fold properly,
• Thus preventing conformational change of gp41 required to complete final step in
fusion process
• Dose 90 mg SC bid
• Dose adjustments are not required in patients with renal insufficiency or mild-to-
moderate hepatic insufficiency
• ADRs Injection-site reactions (eg, pain,erythema, induration, nodules) diarrhea,
nausea,fatigue, hypersensitivity reactions, increased rate of bacterial pneumonia

50. INTEGRASE INHIBITORS (HIV
INTEGRASE STRANDTRANSFER
INHIBITORS)• HIV integrase
• Responsible for transport and attachment of proviral DNA to host-cell chromosomes,allowing
transcription of viral proteins and subsequent assembly of virus particles.
• Proviral integration involves 2 catalytic reactions:
• 3'-processing in host-cell cytoplasm to prepareproviral strandsfor attachment
• Strand transfer whereby proviral DNA is covalently linked to cellular DNA
• IIs Competitively inhibitstrand transfer reaction by binding metallic ions in active site.
• Raltegravir & Elvitegravir
• Dolutegravir
• Newest integrase inhibitor, is now in very advanced clinical trials, with approval
expected towards the end of 2013.
• once-a-day medication, can be taken separately.
• doesn't require a booster
• appears to work against virus that is resistant to raltegravir and/or elvitegravir.

51. COMMERCIAL FIXED-DOSE
COMBINATIONS
Combination Name
Zidovudine + lamivudine Combivir
Zidovudine + abacavir Epzicom
Zidovudine + lamivudine + abacavir Trizivir (combivir +ABC)
Tenofovir + emtricitabine Truvada
Tenofovir + emtricitabine + efavirenz Atripla (Truvada +EFV)
Stavudine + lamivudine + nevirapine Triomunea
Lopinavir + ritonavir Kaletra
Rilpivirine + tenofovir/emtricitabine Complera
Elvitegravir+ cobicistat+ tenofovir + emtricitabine Stribild

52. TYPES OFTREATMENT FAILURE
• Virologic Failure: if viral load is not <400 copies/mL after 3mo
• Immunologic Failure:
• The CD4 cell count persistently falls below the baseline CD4 cell
count
• The CD4 cell count fails to increase by more than 25-50 cells/μL after
one year of treatment
• There is a > 50% decline in CD4 cell count from its highest level on
ART
• Clinical Failure:
• when the patient has a newAIDS-defining illness—i.e.,a newWHO stage
3 or 4 condition--after initiation of ART

55. Thank You

57. Name Dosage Form(s) Adult Dose Adverse Events
Raltegravir 400-mg tablet 400 mg PO bid
With rifampin:800
mg PO bid
Nausea, diarrhea,
headache, CK
elevations,
myopathy/rhabdo
myolysis (rare)
Elvitegravir Available in‘quad’
pill,elvitegravir/co
bicistat/emtricitab
ine/tenofovir
(Stribild).
_
nausea,diarrhea,
fatigue,and
headache

58. HIV LATENCY
• Latently infected resting memory CD4+ T cells are the best
characterized latent reservoir for HIV-1.
• Less than 1 cell per 1,000,000 resting CD4+ T cells from
patients on HAART harbor latent HIV-1 provirus.
• Sequence of latent proviruses does not evolve, which
suggests no ongoing viral replication.
• Discontinuation of HAART allows viral relapse from latent
reservoir.

59. HIV LATENCY(CONT.)
• Patients successfully treated with HAART for longer than 10
years exhibit no appreciable decrease in the size of the latent
reservoir.
• The persistence of latently infected memory CD4+ T
lymphocytes precludes their elimination by HAART alone for
the lifetime of the patient.
• Other drug-insensitive reservoirs, including brain,
macrophages, and hematopoietic stem cells, may also exist.
• Latency is likely established and maintained by numerous
blocks at multiple steps in the HIV-1 replicative pathway,
which potentially complicates eradication strategies.

60. HIV LATENCY(CONT.)
many lymphocytes can be
visualized that produce small
amounts of viral RNA, yet
do not display markers of
activation

61. 0 50 100 150
Half-life (Days)
Estimated half-life of HIV-1 infected cells
Finzi & Siliciano, Cell 93:665, 1998
Resting memory CD4+ T cell
with latent HIV provirus
Free virions
Infected
macrophages
Productively infected
CD4+ T cell
Virions trapped on
follicular dendritic cells
Resting CD4+ T cell
with unintegrated virus
RESERVOIRS OF HIV-1 INFECTION

62. PRINCIPLES OF HIV DRUG RESISTANCE
• Results from changes (mutations) in genetic information in virus
• These changes occur whenever HIV is replicating
• Partial HIV suppression promotes resistance
• Resistance can be delayed by suppressing virus completely
• RT and protease are flexible (highly mutable)
• Resistance may fade but not disappear when a drug is stopped
• Some mutations allow certain viruses to resist effects of one or more
antiretroviral drugs
• Drug resistant virus usually grows faster and better than drug susceptible virus
• Drug resistant virus replaces drug susceptible virus in patient

63. 63
MINIMIZE EMERGENCE OFVIRAL
RESISTANCE
• Never prescribeARVs in absence of adherence counseling
and support
• Never prescribe monotherapy or dual therapy
• Ensure optimal serum drug concentrations
• Avoid drug interactions
• Diagnose and manage malabsorption
• IfARV medications are to be discontinued,stop all drugs at
same time
• Possible exception: NNRTI-based regimen

64. HAART is no panacea.
Current treatments must be maintained for life
with treatment interruption resulting in the rapid
rebound of replicating virus
Although drug resistance can emerge

65. PRINCIPLES OF HIV DRUG RESISTANCE
• Results from changes (mutations) in genetic information in virus
• These changes occur whenever HIV is replicating
• Partial HIV suppression promotes resistance
• Resistance can be delayed by suppressing virus completely
• RT and protease are flexible (highly mutable)
• Resistance may fade but not disappear when a drug is stopped
• Some mutations allow certain viruses to resist effects of one or more antiretroviral
drugs
• Drug resistant virus usually grows faster and better than drug susceptible virus
• Drug resistant virus replaces drug susceptible virus in patient

66. RESISTANCETESTING
• Two types:
• Genotyping
Detects drug resistance mutations on virus genome that may make it
resistant to certain antiretrovirals
• Less expensive
• Can usually be completed in 1-2 weeks
• Phenotyping
Measure ability of viruses to grow in presence of various
concentrations of antiretroviral drugs
• More expensive
• Generally takes 2-3 weeks to complete

67. 67
Resistance Mutations
• For some drugs (NNRTIs and 3TC), a single mutation causes high-level
resistance.
• Resistance to these drugs occurs very quickly
• For other drugs (most NRTIs and PIs), many mutations must occur before
high-level resistance is observed.
• Resistance to these drugs occurs more slowly
Cross-Resistance
• Resistance to one drug can cause resistance to others of the same class
• NNRTI: complete cross-class resistance
• NRTI: partial cross-class resistance
• PI: partial cross-class resistance
• Partly overcome by ritonavir boosting

68. 68
MINIMIZE EMERGENCE OFVIRAL
RESISTANCE
• Never prescribeARVs in absence of adherence counseling
and support
• Never prescribe monotherapy or dual therapy
• Ensure optimal serum drug concentrations
• Avoid drug interactions
• Diagnose and manage malabsorption
• IfARV medications are to be discontinued,stop all drugs at
same time
• Possible exception: NNRTI-based regimen

69. Despite the prolonged suppression of HIV
replication below the standard limits of detection for
patients on HAART, ongoing viremia can be detected
at levels of 1 to 50 copies per milliliter in the
majority of patients
The origin of this viremia has not been fully
characterized

70. PURGING PERSISTENT PROVIRAL
INFECTION

75. WHY DO WE NEED VACCINE FOR HIVWHILE
INFECTION COULD BE CONTROLLED BY ARV
THERAPY ?
 The suboptimal penetration of many antiretrovirals into the
central nervous system may also permit low levels of viral
replication and/or release from stable viral reservoirs,resulting
in neuropathology
 There is already growing concern about increased rates of heart
disease,diabetes,liver disease,and many forms of cancer in aging
HIV-infected patients who are receiving treatment
 the cost of HAART may be too much to sustain treatments on a
global scale,as millions are affected

76. AN IDEALVACCINE SHOULD BE ….
• Good immune response
• Both Cell Mediated Immunity and antibody responses.
• Immunity is long lived
• Single dose
• Safety
• Danger of reversion to virulence,or Severe disease in immunocomprised
• Stability
• Organisms in the vaccine must remain viable in order to infect and
replicate in the host
• Vaccine preparations are therefore very sensitive to adverse storage
conditions
• Maintenanceof the cold chain is very important.
• Expense
• Cheap to prepare

77. ANTI HIV AGENTS UNDERTRIALS
• Nucleosides- DAPD,DOTC,GW-42086,D-D4FC
• Non-nucleosides- DPC 961,DPC 083,Capravirine,CalanolideA,
TMC 120
• PI’s- BMS 232632,AG 1776,DMP 450,CGP61755,DPC
681,DPC 684,TMC 126
• Fusion Inhibitors -T- 1249
• Interleukin-2
• Vaccine development- vCP1452,gp-160
• Integrase Inhibitors- DCQA/DCTA,Zintevir
• Hydroxyurea-like Compounds- BCX-34,