To know the major causes of
this disease, how it is transmitted, and understand the basic processes
that result in the progression from HIV infection to AIDS.
Specific Educational Objectives:
The student should be able
1. recite the most likely causes of
HIV/AIDS and how this viral infection is usually acquired in the United
States (modes of transmission for females and males are different).
2. describe how the virus attaches to
human cells. Also know the human cell receptors that the virus attaches
to (hint: M-tropic vs. T-tropic viruses).
3. describe the three different
HIV/AIDS disease stages and what happens to the immune system during
those disease stages.
4. describe the various means of
diagnosing HIV/AIDS and when to use which test. You should also know
CDC's definition for AIDS.
5. list the most common opportunistic
infections that occur in HIV/AIDS patients.
5. describe the basic treatment regimen
6. list ways of preventing HIV
infections (hint: how do you prevent congenital infections?)
C.P. Conlon and D.R. Snydman, Mosby's
Color Atlas and Text of Infectious Diseases. Mosby, 2000. Chapter 13,
Dr. Neal R. Chamberlain
A wonderful and informative website to visit is from Johns
Hopkins Medical Center Called "The Body". Go there you will learn alot!
Good article at Webpath on HIV and AIDS.
An extensive review of HIV/AIDS vaccines and the basic science
findings: NIH-Funded AIDS Vaccine Research: A Critical Review by
Gregg Gonsalves. For recent updates on vaccines go to
Chen RY, Kilby JM, and Saag MS. Enfuvirtide. 2002 Expert. Opin.
Investig. Drugs. Dec;11(12):1837-43.
Immunodeficiency Syndrome (AIDS) is currently a growing, worldwide,
fatal, pandemic. Destruction of CD4+ T cells predisposes infected
individuals to a wide range of opportunistic infections, tumors,
dementia and death.
"The reality of AIDS in Botswana is so
grim it is hard to grasp. In the main hospital in the capital city,
Gaborone, 70% of beds in the pediatric ward are for children with
complications of AIDS. The medical ward varies from 60-80%. Sometime
this year, it is projected we will have 70,000 orphans, in a country
with a population of 1.5 million people. One village of 30,000 people
recently had 42 funerals in one weekend, with people having to choose
whose funeral they would attend. Yet in that same village, a
once-thriving orphan-care program struggles for funds, even for food for
the children being cared for. One grandmother has lost all her siblings
and their partners, leaving her with more than 20 young children to care
for. This is in a society that used to care for its elderly within the
extended family. True infection rates are closer to 30% (as reported in
the January 17 issue of Newsweek), with most infections in the 15-49 age
group. Life expectancy has dropped from 67 years to somewhere around 50
years, and is expected to drop as low as 40 years during the next ten
years." (AIDS Survival News; A Letter from Africa. A First-Hand of
Account of How AIDS Has Affected the People of Botswana By H. Ruth
Human immunodeficiency virus (HIV) types 1 and 2, human
retroviruses, lentivirus subfamily. HIV is the causative agent of AIDS.
The most common type is HIV-1 and is the infectious agent that has led
to the worldwide AIDS epidemic. HIV-2 infection is less common and less
virulent, but results in AIDS as well.
worldwide) and HIV-2 (mainly endemic in west Africa) were first isolated
and associated with the disease in 1982 and 1983.
AIDS was first recognized in 1981,
although retrospective studies suggest that cases occurred in Africa in
the 1950's and in the U.S. by the 1970's.
Currently, two principal genetic groups
of HIV-1, designated M (main) and O (outlier), have been identified.
Genetic group M is highly prevalent and is further classified into 10
established envelope subtypes, A through J. HIV-1 subtype B predominates
in Europe and the Americas, whereas HIV-1 subtype C predominates
sub-Saharan Africa. Mosaic forms, which combine the genetic material
from two distinct subtypes, have also been identified.
Living with HIV/AIDS
Africa and Middle East
Eastern Europe and Central Asia
Australia and New Zealand
* as of end of 1998
In contrast to HIV-1 infection, which
has spread through all continents, HIV-2 is primarily restricted to West
Africa and to population movements from or through this region. HIV-2
strains are classified into five subtypes, A through E; only subtypes A
and B viruses are predominant.
Other inflammatory STD's enhance HIV transmission. These infections
include syphilis, gonorrhea, genital herpes, etc.
Infection is aided by Langerhans cells
in mucosal epithelial surfaces which can become infected. Infection is
also aided by the presence of other sexually transmitted diseases
that can produce mucosal ulceration and inflammation. The CD4+
T-lymphocytes have surface receptors to which HIV can attach to promote
entry into the cell. The infection extends to lymphoid tissues (MALT)
which contain follicular dendritic cells that can become infected and
provide a reservoir for continuing infection of CD4+ T-lymphocytes.
Transmission is intracellular: HIV
transmission most likely requires HIV-infected cells, such as
macrophages, lymphocyte or spermatozoa, which enter the body through
microabrasions of the mucous membranes or through penetration of the
skin with a needle.
Transmission via free virus appears to
Modes of transmission:
contact (heterosexual (most common means in the world) and
- blood or
blood product transfusion (before routine testing)
tissue (before routine testing)
- IV drug use
with shared needles
transplacental (in utero) or by perinatal infection of
neonates (breast milk).
About 33.4 million people are infected
with HIV/AIDS, worldwide (1999). The highest rates of infection are in
sub-Saharan Africa where 1 in 20 men and 1 in 20 women are estimated to
Click on image for an enlarged view.
In the United States, AIDS is the 5th
leading cause of death in people 25-44 years of age. 753,907 cases of
AIDS have been reported since 1981; CDC). There are 120,223
patients living with HIV infection in the U.S. (2000; CDC).
311,701 people are living with AIDS in the U.S.. 438,795 people have
died of AIDS in the U.S. (before 1981-2000; CDC). 21,016 new HIV
infections were diagnosed in 2000 (33% female; 67% male; CDC).
43,293 new cases of AIDS were diagnosed in 2000 (CDC).
Deaths due to AIDS:
High risk populations (1999; CDC):
MALES (new cases
of AIDS; 1999):
11,021 new cases
homosexual men (MSM; men having sex with other men) 71%
IV drug abusers (IDU) 14%
MSM and IDU 8%
heterosexual contact 5%
6,714 new cases
heterosexual contact 7%
and IDU 7%
14,103 new cases
heterosexual contact 18%
and IDU 8%
cases of AIDS; 1999):
1,796 new cases
heterosexual contact 55%
1,826 new cases
heterosexual contact 47%
6,539 new cases
heterosexual contact 50%
Pediatric cases of AIDS:
to mother with or at risk for HIV infection= 88%
of AIDS patients:
25-49 y - 85% of cases
13-19 y - <1% of cases
y - ~2% of cases
Racial distribution of AIDS in U.S. through December 1999:
white - 38%
African American - 41%, yet 12% of population
Hispanic - 20%, yet 6% of population
other - 1%
most AIDS cases in the U.S. occur in the most populous states and
Figure 1. Female
adult/adolescent annual AIDS rates per 100,000 population,
for cases reported July 1999 through June 2000
Figure 1. Male
adult/adolescent annual AIDS rates per 100,000 population,
for cases reported
July 1999 through June 2000
http://www.cdc.gov/hiv/stats/hasr1102.htm to get the number of cases
in the U.S.
HIV can cross the
epithelial barrier through a process known as transcytosis by M cells
(these cells line the intestine). Once past the epithelia, HIV is
thought to be picked up by antigen presenting cells (APCs), primarily
dendritic cells (DCs). Newer work, however, suggests that HIV directly
infects CD4+ T lymphocytes in mucosal associated lymphoid tissue (MALT),
establishes a fulminant local infection within a few days, and then
spreads quickly throughout the body. Recent data suggest that viral
reservoirs are established early during mucosal infection. Preventive
vaccines must engender a quick and vigorous mucosal immune response.
HIV must bind two surface
proteins to infect a cell, CD4 and CXCR4 (formerly known as fusin), or
If CD4 and CXCR4 are used, the HIV
virus is T-tropic. T-tropic
viruses are transmitted via blood and blood products. They are
syncytia-inducing viruses and infect T-cells.
If the HIV virus binds to CD4 and
CCR-5, it is M-tropic.
M-tropic viruses are transmitted via sexual contact. They are not
syncytia-inducing viruses and infect macrophages and T-cells.
A pool of latently infected CD4+ T
cells during the very earliest stages of acute HIV infection are
infected by the virus. These infected cells are able to persist in the
patient's body for extremely long periods of time (several years).
CD8+ cells promote CD4+ cell death when
the T-tropic viruses start binding to CXCR4 on the CD8+ cells and with
help from macrophages triggering apoptosis in CD4+ cells.
CD4+ cells are major targets for HIV,
i.e., T helper lymphocytes, monocytes, neurons.
HIV recognizes and binds to the CD4 molecule via viral envelope
glycoprotein gp120, and then binds to CXCR4 or CCR-5. A "schematic
drawing" of gp120 binding to the receptors.
Viral reverse transcriptase
produces complementary DNA using the viral RNA template.
Viral DNA is transported into the nucleus and is integrated into the
chromosome (now called a provirus), where it instigates cytopathic viral
production or possibly effects programmed cell death in non-infected
cells. Diagram of virus "life cycle"
The life cycle of human immunodeficiency virus is diagrammed
here. Note that the reverse transcriptase enzyme makes an HIV
proviral DNA that is incorporated into the host cell.
The course of AIDS
progresses along a series of defined disease stages or classes and
ultimately is fatal.
acute viral infection
period of 1-3 weeks
symptoms, or any or all
of the following "mononucleosis-like symptoms":
- sore throat
- malaise -
rash - small pink papules or macules over much of the body
Stage I ends with
the production of high titers of anti-HIV antibodies at 2-3 months,
postinfection. Anti-HIV antibodies are usually detectable by ELISA by
Lasts for 6 or more years in 65-85% of
Patients produce large amounts anti-HIV
HIV is detectable in blood, semen, and
New PCR procedures show that as many as
1 in 10 peripheral CD4+ cells are infected.
HIV-antibody-complement complexes are
trapped in lymph nodes, tonsils, spleen, etc. by follicular dendritic
CD4+ T cells disappear from the blood
because they are sequestered in the lymph nodes (numbers are 5-10X
higher than in the peripheral blood)
Follicular Dendritic Cells (FDC)
facilitate HIV transmission to uninfected T cells.
When peripheral CD4+ cells number
500-200/µl, the FDC are dying and the internal structure of the lymph
node is breaks down; HIV spills over into the blood.
Severity is directly related to the
decline of CD4+ T cells, which causes diminished function by TC, B cells
(hypogammaglobinemia), macrophages and NK cells, and leads to
opportunistic infections and spontaneous neoplasms.
The individual has a chronic lifelong
Western Blot Analysis
Early Marker of Infection
(detection of a recent infection)
Virion RNA RT-PCR
Detection of virus in blood
(detection of a recent infection) and to confirm treatment
CD4:CD8 T-cell Ratio
Staging the disease and to
confirm treatment efficacy.
Isolation and culture of
Only available in research
Transcriptase-Polymerase Chain Reaction
this antigen is produced early in
infection and is present in the patient's bloodstream. It is useful in
detecting very recent infections and in detecting HIV infection in
neonates of HIV infected mothers. Serological tests can not detect
recently infected individuals.
Polymerase Chain Reaction
(RT-PCR) to detect HIV RNA in plasma. To determine the presence of the
HIV genome during the first 2-4 weeks of infection, when patients may be
seronegative and yet are infective. It is also useful in detecting HIV
infection in neonates. Now used in determining effectiveness of
treatments. In concert with CD4 cell counts PCR helps in determining a
Immunoabsorbent Assay (ELISA)
A screening test for antibody reactive with HIV proteins. ELISA for
HIV-1 or HIV-2 antigens then a Western blot is performed for a
definative diagnosis of HIV infection. Antibody specific for HIV gp120
or gp160 (detectable within 4-8 weeks post-exposure). However in 5% of
the patients antibodies may not be detectable for 6 months or more.
Western blotting To
determine the presence of HIV-specific antibody. To confirm positive
assay (coated with HIV
antigen) To determine the presence of HIV-specific antibody. A new
screening test which is quicker than the ELISA.
Simpler and more
rapid serological tests for HIV are coming out and will be available
To determine if a person that is HIV infected has developed AIDS a
case definition is utilized. Children and infants are little more
difficult to diagnose.
patients with mononucleosis-like symptoms:
generalized lymphadenopathy syndrome (PGL)
multiple enlarged lymph nodes
AIDS-related complex (ARC)
- fever - role
for TNF, IL-1
- weight loss
- night sweats
(seen in long-term
Among the earliest observed AIDS-related conditions occur as infectious
or noninfectious skin eruptions.
Mucosal candidiasis and Thrush (white, non-adherent plaques and
Intertriginous cutaneous candidiasis
Paronychia Dermatophytosis - Tineas:
pedis, cruris, corporis; due to Trichophyton rubrum;
Onychomycosis Disseminated fungal
infections showing early skin lesions
- in endemic areas; pulmonary and renal failure
Herpes simplex non-healing ulcers; genital, perioral, perianal; perform
the Tzanck test
Varicella zoster reactivation within
the dorsal root ganglion
Molluscum contagiosum (pox virus agent)
- umbilicated, skin-colored papules on the face or trunk, confused with
sebaceous hyperplasia, disseminated cryptococcosis, and basal-cell
Warts - pre-existing skin and genital
warts become difficult to treat
Oral hairy leukoplakia - whitish,
corrugated or hairy, adherent plaques, lateral margins of the tongue
Cytomegalovirus - nonhealing perianal
or anal ulcers
Staphylococcus, Streptococcus, Haemophilus, Pseudomonas:
folliculitis, impetigo, cellulitis
Syphilis - rapidly progressing to
tertiary syphilis; secondary syphilis may be seronegative; test
individuals showing a papulosquamous rash with RPR and/or a silver stain
of a skin biopsy
and avium-intracellulare skin lesions at the site of injections
Noninfectious inflammatory diseases:
Seborrheic dermatitis - most common cutaneous manifestation; 3% of the
general pop., 85% of the HIV+ pop.; often associated with Malassezia
Psoriasis - exacerbation of existing
Other inflammatory dermatitis -
scabies, atopic dermatitis
Malignant neoplasms of the skin:
Kaposi's sarcoma - pink to red to purple to brown, anywhere on skin;
(1984) HHV8 also called Kaposi's sarcoma herpes virus (KSHV) has a
causal role; treatment may not affect survival
Lymphoma - Hodgkin's, non-Hodgkin's,
Invasive cervical cancer
Other cutaneous manifestations:
Epithelioid angiomatosis - violaceous papules and nodules resembling
Hair changes - greying, hairline
Yellow nail syndrome
May have multiple infections.
pneumocystosis - damaged alveoli with cyst production.
This airborne fungus is often acquired
in childhood as evidenced by specific antibody. Latent infections are
reactivated in adults with a severe T-cell deficiency or in children
with a moderate T-cell deficiency. Shortness of breath, fever,
weight-loss, dry non-productive cough, interstitial infiltrate in both
lungs. P. carinii is identified by its characteristic morphology
with a Giemsa stain of an induced sputum sample or a sample from a
bronchial alveolar lavage; culture of this organism is difficult.
Cytomegalovirus: interstitial pneumonia
Oral, anal, and esophageal inflammation
Herpes simplex virus;
oral thrush and esophagitis;
Epstein-Barr virus: oral hairy
Severe diarrhea and malabsorption of
(another picture of Cypto. and a fecal smear: acid fast stained)
and M. intracellulare
Lymphadenopathy or lymphadenitis
Retinitis and blindness cytomegalovirus
Toxoplasma gondii: toxoplasmosis Cryptococcus neoformans:
Therapy for HIV
Eradication of HIV infection cannot
be achieved with currently available antiretroviral regimens therefore
treatment to suppress the virus is lifelong. This is because a pool of
latently infected CD4+ T cells during the very earliest stages of acute
HIV infection persists with an extremely long half-life, even with
prolonged suppression of plasma viremia to < 50 copies/mL. Treatment has
resulted in substantial reductions in HIV-related morbidity and
The primary goals of antiretroviral
maximal and durable suppression of viral load,
restoration and/or preservation of immunologic function,
improvement of quality of life,
reduction of HIV-related morbidity and mortality.
(Highly Active Antiretroviral Therapy)- therapy, available since 1995,
has resulted in durable antiviral responses that are being observed in
an increasing number of patients. Many benefits of long term therapy are
being reported. Successful HAART results in suppression of viral
replication and halts damage to the immune system. It also partially
restores the immune system leading to partial restoration of immune
function. Clinical benefits accompanying these immunologic benefits
include fewer opportunistic infections and longer life for the patients.
Conclusion: The amount of virus in the blood stream is significantly
lowered and lowered for long periods of time in patients treated with
all three drugs.
With the increased use of PI's the number of deaths due to AIDS can be
Classes of anti-retroviral drugs:
1. Nucleoside/Nucleotide Reverse
Transcriptase Inhibitors (NRTI's)
NRTIs were the first group of
antiretriviral drug approved for use in HIV/AIDS patients. NRTIs inhibit
HIV's reverse transcriptase and can be placed within the viral DNA. When
the NRTI's are placed in the viral DNA by the reverse transcriptase
transcription of the viral genes is inhibited. This prevents virus
multiplication and subsequent spread of the viral infection. Nucleosides
require phosphorylation before they can affect reverse transcriptase
activity. This phosphorylation occurs via host enzymes. The nucleotides
are already phosphorylated and do not need to be activated to inhibit
the viral enzyme.
2. Non-Nucleoside Reverse
Transcriptase Inhibitors (NNRTI's)
These drugs also inhibit reverse
transcriptase which prevents virus multiplication and spread. They do it
in a slightly different fashion than NRTI's.
3. Protease Inhibitors (PI's)
HIV produces its own protease that is
important in the production of infective viral particles. The protease
cleaves the viral proteins to the correct sizes so that a mature viral
particle can be formed (viral assembly). The protease inhibitors inhibit
the retroviral protease from cleaving the viral proteins. These drugs
help to slow the spread of the virus to other uninfected cells. Do
not use protease inhibitors in monotherapy. HIV quickly becomes
resistant to the protease inhibitors.
4. Fusion inhibitors: A new class of
drugs is currently approved for use in AIDS patients.
The drug Enfuvirtide [T-20, pentafuside, Fuzeon (trade name)], is a 36
amino acid peptide that mimics one section of gp41. This peptide
inhibits virion-host cell fusion. Gp41 is essential in getting the HIV
virion into the host cell. Refer to figure below.
With very few adverse reactions twice a
day subcutaneous injections of Enfuvirtide resulted in significant
reduction in viral load (about a 1 log reduction) at 24 weeks. This drug
was recently (3/03) approved by the FDA for use in patients in the
United States. This drug cannot be used alone it must be used with other
anti-HIV drugs and is only recommended for patients with HIV-1 virus
that is resistant to the other antivirals.
Another fusion inhibitor is also in the
pipeline and should soon be approved by the FDA. It is a 39 amino acid
peptide (T-1249) that binds to gp41 in a slightly different place than
The following information was taken
from: Antiretroviral Therapy for HIV Infection in 1998; Updated
Recommendations of the International AIDS Society–USA Panel. ("JAMA".
Vol. 280, pp. 78-86, Jul. 1, 1998.)
Early treatment of HIV infection has
delayed the progression to AIDS. However, certain things should be
considered as complicating this picture:
virologic response rates to initial therapy with a PI and 2
nucleoside reverse transcriptase inhibitors (nRTIs) range from 60% to
90% and success of initial therapy is less likely as the disease
durability of viral suppression beyond 2 years is uncertain;
however if viral titers increase studies have shown less opportunitic
infections in people who remain on HAART.
close drug adherence is essential in preventing viral resistance,
and current regimens are difficult;
drug interactions resulting from hepatic metabolism of PIs and
nonnucleoside reverse transcriptase inhibitors (NNRTIs) increase
impact of extended treatment on quality of life is a major
new and long-term adverse effects are appearing, particularly
with PI-containing regimens.
Therapy should be Started:
There is growing consensus, as
represented by recommendations of a Department of Health and Human
Services (DHHS)-appointed panel, that early
treatment initiation is associated with virologic, immunologic,
and clinical benefits. The International AIDS Society–USA panel
continues to recommend antiretroviral therapy for any patient with
established HIV infection and a confirmed plasma HIV-1 RNA level greater
than 5000 to 10,000 copies/mL who is committed to the complex, long-term
therapy. Accumulating data show that viral load is a strong, independent
predictor of clinical outcome. Degree and durability of virologic
response correlate directly with plasma HIV RNA level and CD4+ cell
count at baseline. Treatment options should be discussed with all
patients with HIV infection.
Pretreatment plasma HIV RNA level and
CD4+ cell count are important for evaluation of response to treatment.
In general, prior to therapy initiation, 2 plasma viral load levels
using the same technology and 2 CD4+ cell counts should be obtained at 2
separate visits, at which times drug therapy options, implications, and
requirements are discussed and reviewed.
For asymptomatic patients with low
plasma HIV RNA level (eg, <5000-10,000 copies/mL) and high CD4+ cell
count (eg, >0.35-0.50 × 109/L [350-500/µL]) deferral of
therapy with close follow-up may be appropriate given treatment
complexities, risk of adverse effects, consequences of resistance, and
the possibility that such persons may fall into the category broadly
described as long-term nonprogressor. For those with low HIV RNA level
(eg, <5000-10,000 copies/mL) and low CD4+ cell count (eg, <0.50 × 109/L
and particularly <0.35 × 109/L), therapy initiation is
recommended, given independent prognostic significance of CD4+ cell
count and clinical trial data support.
Another approach is to treat
symptomatic patients and patients in category 3 (CD4+ cell count <200/ul).
Encourage treatment for asymptomatic patients in category 2 and wait to
treat asymptomatic patients in category 1.
Initial Antiretroviral Regimens:
The goal of antiretroviral therapy is
to improve survival and decrease morbidity via continuous
maximum suppression of HIV replication.
There are currently three types of
combination regimens employed as initial treatment (no prior
NNRTI-based regimens (one NNRTI and 2 nRTIs) that are PI sparing
(ex. efavirenz + zidovudine + lamivudine).
A recent study, ACTG 384, indicates that certain combinations of these
drugs are better in patients with no prior HIV treatment (Robbins GK et
al. Comparison of sequential three-drug regimens as initial therapy for
HIV-1 infection. N Engl J Med. 2003;349:2293-2303). Researchers
in this study found that efavirenz (EFV) + zidovudine (AZT) + lamivudine
(3TC) were the best at preventing treatment failure.
PI-based regimens that are NNRTI sparing (1 or 2 PIs + 2 or 3
nRTIs; ex. )
Triple nRTI regimens that are both PI- and NNRTI-sparing (ex.
lopinavir/ritonavir + lamivudine + zidovudine)
Use of potent therapy has resulted in
remarkable declines in hospitalization rates, morbidity, and mortality
where the drugs are available. Furthermore, protease inhibitor
(PI)-containing regimens can be cost-effective.
There are 20 approved antiretroviral
drugs so far:
8 nRTIs [abacavir, emtricitabine (FTC),
zidovudine (AZT), didanosine (DDI), zalcitabine (DDC), lamivudine
(3TC), tenofovir (disoproxil fumarate), and stavudine (D4T)]
3 NNRTIs (efavirenz (EFV),
nevirapine and delavirdine)
8 potent PIs (amprenavir, atazanavir,
indinavir, lopinavir/ritonavir, nelfinavir (NFV), and saquinavir
Fusion inhibitor (Enfuvirtide)
Monitoring Response to Therapy:
Plasma viremia is a strong prognostic
indicator in HIV infection. The higher the levels of HIV RNA in the
patient's bloodstream the worse their prognosis. HAART often leads to
increases in the CD4+ T cell count of 100-200 cells/ml or more. CD4+ T
cell responses are generally related to the degree of viral load
Plasma HIV RNA assays of increased
sensitivity, which have a dynamic range of about 20 to 50 to about
50,000 copies/mL of plasma should be used to determine success of
treatment and treatment failures. Every 2 months plasma HIV RNA levels
and CD4+ cell counts should be obtained. When CD4+ cell count decline
occurs in concert with a rising HIV RNA level in an adherent patient,
there is no question that treatment failure has occurred.
Treatment to reduce transmission of
HIV-1 to infants born to pregnant women infected by HIV-1.
TABLE 1. Pediatric AIDS
Clinical Trials Group (PACTG) 076 zidovudine (ZDV) regimen
Time of ZDV
Oral administration of 100 mg ZDV five times daily,
initiated at 14-34 weeks' gestation and continued throughout
During labor,intravenous administration of ZDV in a 1-hour
initial dose of 2 mg/kg body weight,followed by a continuous
infusion of 1 mg/kg body weight/hour until delivery.
Oral administration of ZDV to the newborn (ZDV syrup at 2
mg/kg body weight/dose every
6 hours) for the first 6 weeks of
life, beginning at 8-12 hours after birth. (Note:
intravenous dosage for infants who can not tolerate oral
intake is 1.5 mg/kg
body weight intravenously every 6 hours.)
Service Task Force Recommendations for the Use of Antiretroviral Drugs
in Pregnant Women Infected with HIV-1 for Maternal Health and for
Reducing Perinatal HIV-1 Transmission in the United States,
Morbidity Mortality Weekly Report; Recommendations and Reports. January
30, 1998 / 47(RR-2);1-30
If a single dose of Nevirapine is given
to mother during labor and a single dose of Nevirapine is given to the
neonates after delivery in addition to the ZDV treatment above the rate
of transmission of HIV to the infant decreased to about 1 percent (ZDV
plus Nevirapine) verses around 6 percent (ZDV only). (Lallemant et. al.
2004. Single-dose perinatal nevirapine plus standard zidovudine to
prevent mother-to-child transmission of HIV-1 in Thailand. N. Engl. J.
Med. Jul 15;351(3):217-28).
Safe sex, safe use
of needles and more effective early screening. Treat HIV-1 infected
pregnant women as indicated above to prevent infection of the
Vaccines: No vaccine is currently
approved by FDA. Clinical
trials are currently being conducted with a number of different
Send comments and email to Dr. Neal R.