What is HIV? HIV stands for Human Immunodeficiency Virus.

HIV destroys certain white blood cells called CD4+ T cells. These cells are critical to the
normal function of the human immune system, which defends the body against illness.When
HIV weakens the immune system, a person is more susceptible to developing a variety of
cancers and becoming infected with viruses, bacteria and parasites.

What is AIDS? AIDS stands for Acquired Immunodeficiency Syndrome.

A person who tests positive for HIV can be diagnosed with AIDS when a laboratory test
shows that his or her immune system is severely weakened by the virus or when he or she
develops at least one of about 25 different opportunistic infections -- diseases that might not
affect a person with a normal immune system but that take advantage of damaged immune
systems.
How long does it take for HIV to cause AIDS?
The time between HIV infection and progressing to AIDS differs for each person and
depends on many factors, including a person's health status and their health-related
behaviors. With a healthy lifestyle, the time between HIV infection and developing AIDS-
related illnesses can be 10 to 15 years, sometimes longer. Antiretroviral therapy can slow
the progression of HIV to AIDS by decreasing the amount of virus in a person's body.
How does HIV cause AIDS?
HIV destroys CD4+ T cells that are important to the normal function of the human immune
system. As the virus destroys these cells, HIV-positive people are susceptible to illnesses
that generally do not affect people with healthy immune systems.According to studies
including thousands of people, most HIV-positive people are infected with the virus for years
before it does enough damage to the immune system to make them susceptible to AIDS-
related diseases.

Study case
In 5 patients the AD preceded HIV infection. Mean follow-up before HIV infection was 5
years (1;10) and afterwards 13 years (2;19). The diseases were: lupus, Graves disease, RA,
sarcoidosis, and APS/systemic lupus. In 14 patients, HIV infection was diagnosed at the
same time as the AD. Mean follow-up of these diseases was of 8.35 years (1;27). The
diseases were: vasculitis (7/11 patients), APS (2/4 patients), ITP (2/6 patients),autoimmune
hepatitis (1/4 patients), RA/lupus (1/1 patient),and sarcoidosis (1/7 patients). For the 13
patients for which data were available, mean CD4 T lymphocyte count and percentage at
HIV and AD diagnosis were 326/mm3 (83;716) and 21.3% (10;35); the CD4/ CD8 T
lymphocytes ratio was superior to 1 in one patient (Table 2). Thirty-four patients were HIV-
infected when they developed an AD. Mean follow-up before AD diagnosiswas 9 years
(1;20) and afterwards 5.8 years (0.25;22). At AD diagnosis, all patients received antiretroviral
(ARV) treatment except for 7 of them (for one patient data was not available); mean CD4 T
lymphocyte count and percentage were 404.2/mm3 (16;900) (for 2 patients data was not
available) and 24.6% (5;59) (for 5 patients data was not available); CD4/CD8 T lymphocytes
ratio was superior to 1 in 7 patients; and HIV viral load was detectable for 10 of them (for 2
patients data was not available) (Table 2).
Clinical Manifestation of the case

Fifty-two patientswere included, ofwhom31werewomen. Follow up took place between 1983

and 2013. Mean age at autoimmune disease diagnosis was 40.1 years (11;59) and at HIV
infection diagnosis 34.4 years (17;64). One patient was an HIV elite controller and one
patient was infected by type 2 HIV; 3 patients had a positive HBs antigen and 6 were
hepatitis C virus (HCV) coinfected. 4 patients presented 2 autoimmune diseases:
antiphospholipid syndrome (APS)/systemic lupus, Graves disease/rheumatoid arthritis (RA)
associated to lupus, Graves disease/cutaneous lupus, and RA/immune thrombocytopenia
(ITP).

Lab test procedure

Study design: retrospective descriptive study. Inclusion criteria: existence of an HIV infection
and an AD. Diagnosis of the AD was done using the usual criteria. Analysis concerned only
patients whose pathology was present in at least 4 patients. Setting: the study took place in
14 medical departments in the Paris and Ile-de-France areas (7 departments of internal
medicine, 2 departments of infectious diseases, 2 departments of clinical immunology, 1
clinical investigation centre, 1 nephrology department and 1 pneumology department).
Screening was realized using an informatic systemwhen available in these departments
and/or by asking directly the physicians. The study was approved by the Aulnay Hospital
Ethics Committee. After patient information, anonymized data available in their medical files
were analysed. Data analysed: demographic data (age, gender); HIV infection history
(diagnosis date, HBV and/or HCV coinfection, immunovirological evolution, treatment); and
AD history (diagnosis date, immunovirological context at diagnosis, treatment, complications
of these treatments, evolution). Complete remission of the ADwas defined as the absence of
any sign of disease activity; partial remission was defined as a significant improvement in
disease signs with persistence of clinical and/or biological signs of disease activity.
Sign and symptoms of HIV infection and AIDS:
Once infected with HIV, a person may or may not experience any symptoms. People who do
experience symptoms might have a flu-like illness within one or two months after infection. 
Symptoms can include
The signs of AIDS include:
 Thrush (a thick, white coating on your tongue or mouth)
 Sore throat
 Bad yeast infections
 Chronic pelvic inflammatory disease  
 Getting bad infections a lot
 Feeling really tired, dizzy, and lightheaded
 Headaches, fever
 Losing lots of weight quickly
 Bruising more easily than normal
 Having diarrhea, fevers, or night sweats for a long time
 Swollen or firm glands in your throat, armpit, or groin
  Deep, dry coughing spells
 Feeling short of breath
 Purplish growths on your skin or inside your mouth
 Bleeding from the mouth, nose, anus, or vagina
 Skin rashes
 Feeling very numb in your hands or feet, losing control of your muscles and reflexes,
not being able to move, and losing strength in your muscles

Specific Symptoms to Men and Women

Both men and women experience many of the same symptoms from HIV infection. However,
women also experience unique complications that are primarily gynecologic. These could
include recurrent vaginal yeast infections, severe pelvic inflammatory disease (PID) or
human papillomavirus (HPV) infections.  Other vaginal infections might occur more
frequently and with greater severity in HIV-positive women (compared with HIV-negative
women), including bacterial vaginosis and common sexually transmitted infections such as
gonorrhea, chlamydia, and trichomoniasis.  HIV-positive women also might experience
disruptions or other irregularities in their menstrual cycles.
Transmission:
You can get or transmit HIV only through specific activities. Most commonly, people get or
transmit HIV through sexual behaviors and needle or syringe use.
Only certain body fluids—blood, semen, pre-seminal fluid, rectal fluids, vaginal fluids, and
breast milk—from a person who has HIV can transmit HIV. These fluids must come in
contact with a mucous membrane or damaged tissue or be directly injected into the
bloodstream (from a needle or syringe) for transmission to occur. Mucous membranes are
found inside the rectum, vagina, penis, and mouth.
In the United States, HIV is spread mainly by
 Having anal or vaginal sex with someone who has HIV without using a condom or
taking medicines to prevent or treat HIV.
o For the HIV-negative partner, receptive anal sex (bottoming) is the highest-
risk sexual behavior, but you can also get HIV from insertive anal sex
(topping).
o Either partner can get HIV through vaginal sex, though it is less risky for
getting HIV than receptive anal sex.
 Sharing needles or syringes, rinse water, or other equipment (works) used to prepare
drugs for injection with someone who has HIV. HIV can live in a used needle up to 42
days depending on temperature and other factors.
Less commonly, HIV may be spread
 From mother to child during pregnancy, birth, or breastfeeding. Although the risk can
be high if a mother is living with HIV and not taking medicine, recommendations to
test all pregnant women for HIV and start HIV treatment immediately have lowered
the number of babies who are born with HIV.
 By being stuck with an HIV-contaminated needle or other sharp object. This is a risk
mainly for health care workers.
In extremely rare cases, HIV has been transmitted by
 Oral sex—putting the mouth on the penis (fellatio), vagina (cunnilingus), or anus
(rimming). In general, there’s little to no risk of getting HIV from oral sex. But
transmission of HIV, though extremely rare, is theoretically possible if an HIV-positive
man ejaculates in his partner’s mouth during oral sex. To learn more about how to
lower your risk, see CDC’s  Oral Sex and HIV Risk.
 Receiving blood transfusions, blood products, or organ/tissue transplants that are
contaminated with HIV. This was more common in the early years of HIV, but now
the risk is extremely small because of rigorous testing of the US blood supply and
donated organs and tissues.
 Eating food that has been pre-chewed by an HIV-infected person. The contamination
occurs when infected blood from a caregiver’s mouth mixes with food while chewing.
The only known cases are among infants.
 Being bitten by a person with HIV. Each of the very small number of documented
cases has involved severe trauma with extensive tissue damage and the presence of
blood. There is no risk of transmission if the skin is not broken.
 Contact between broken skin, wounds, or mucous membranes and HIV-infected
blood or blood-contaminated body fluids.
 Deep, open-mouth kissing if both partners have sores or bleeding gums and blood
from the HIV-positive partner gets into the bloodstream of the HIV-negative partner.
HIV is not spread through saliva.

Laboratory Diagnostics:
1. Serology - the diagnosis of HIV infection is usually based on serological tests.
(a) Antibody tests - ELISAs are the most frequently used method for screening of blood
samples for HIV antibody. The sensitivity and specificity of the presently available
commercial systems approaches 100% but false positive and false negative reactions occur.
Other test systems available include passive particle agglutination, immunofluorescence,
Western blots and RIPA bioassays. Western blots are regarded as the gold standard and
seropositivity is diagnosed when antibodies against both the env and the gag proteins are
detected. The sensitivity of the test systems are currently being improved by the use of
recombinant antigens. 
(b) Antigen tests - HIV antigen can be detected early in the course of HIV infection before
the appearance of antibody. It is undetectable during the latent period (antigen-antibody
complexes are present) but become detectable during the final stages of the infection. It was
argued that the routine use of antigen screening tests in the blood transfusion service may
result in earlier cases of HIV infection being identified. However a large scale study carried
out in the US failed to show any benefit.
2. Virus isolation - virus isolation is accomplished by the cocultivation of the patient's
lymphocytes with fresh peripheral blood cells of healthy donors or with suitable culture lines
such as T-lymphomas. The presence of the virus can be confirmed by reverse transcriptase
assays, serological tests, or by changes in growth pattern of the indicator cells. However
virus isolation is tedious and time consuming (weeks) and is successful in only 70 to 90% of
cases. Therefore virus isolation is mainly used for the characterization of the virus.
3. Demonstration of viral NA - this can be accomplished by probes or by PCR techniques.
The latter may be useful because of its extremely high sensitivity.
4. Prognostic Tests - the following may be useful as prognostic tests; (1) HIV antigen (2)
Serial CD4 counts (3) Neopterin (4) B2-microglobulin. (5) Viral load. Of these tests, only serial
CD4 counts and HIV viral load are still routinely used.
a. HIV viral load - It appears that HIV viral load has the greatest prognostic value. HIV viral
load in serum may be measured by assays which detect HIV-RNA e.g. RT-PCR, NASBA, or
bDNA. HIV viral load has now been established as having good prognostic value, and in
monitoring response to antiviral chemotherapy. Patients with a low viral load during the
incubation period had a better prognosis than those with a high viral load. Patients whose
viral load decreased significantly following the commencement of antiviral therapy had a
better prognosis than those who did not respond.Among patients who responded to antiviral
therapy, those who had a low pre-treatment viral load had a better prognosis than those who
had a high pre-treatment viral load.
b. CD4 counts - despite the increasing use of HIV-RNA assays, measurement of CD4 still
has important value in monitoring disease progression and response to antiviral
chemotherapy. whereas CD4 count gives an indication of the stage of disease. “The
measurement of  HIV viral load tells us where the disease is going, whereas CD4 count tells
us where the disease is at this moment” 
 
5. Antiviral susceptibility assays
Because of the increasing range of anti-HIV agents available, there is increasing pressure
on the provision of antiviral susceptibility assays. There are two types of antiviral
susceptibility assays: phenotypic and genotypic assays
Phenotypic assays define whether a particular strain of virus is sensitive or resistant to an
antiviral agent by determining the concentration of the drug needed to inhibit the growth of
virus in vitro. e.g. Plaque-reduction assay for HSV, plaque-reduction assay for HIV.
However, phenotypic assays can only be used for viruses that can be cultivated. Moreover,
in the case of HIV, plaque reduction assays may not be that appropriate since not all HIV
strains produce plaques in cell culture.
In the case of genotypic assays, mutations that are associated with resistance are assayed
for by molecular biology methods such as PCR and LCR.  However, these assays are
tedious and are not suitable for a routine diagnostic laboratory. Moreover, he results of
genotypic assays may prove very difficult to interpret since HIV mutates at a furious pace,
and it is also possible that resistant strains are present right at the beginning of infection.
Prevention: including

1) prevention and treatment of substance use and mental disorders; 2) outreach

programs; 3) risk assessment for illicit use of drugs; 4) risk assessment for
infectious diseases; 5) screening, diagnosis, and counseling for infectious
diseases; 6) vaccination; 7) prevention of mother-to-child transmission of
infectious diseases; 8) interventions for reduction of risk behaviors; 9) partner
services and contact follow-up; 10) referrals and linkage to care; 11) medical
treatment for infectious diseases; and 12) delivery of integrated prevention
services. These strategies are science-based, public health strategies to
prevent and treat infectious diseases, substance use disorders, and mental
disorders. Treatment of infectious diseases and treatment of substance use
and mental disorders contribute to prevention of transmission of infectious
diseases. Integrating prevention services can increase access to and
timeliness of prevention and treatment.
Treatment:
Therapy of HIV is complicated by the fact that the HIV genome is incorporated into the host
cell genome and can remain there in a dormant state for prolonged periods until it is
reactivated. Effective therapy must be directed against both free virus and virus-infected
cells. Although a number of substances with in vitro anti-HIV activity have been described,
only a few drugs exhibit anti-HIV activity in vivo at tolerable toxicities.
The main group of substances described are:
1. Nucleoside analogues reverse transcriptase inhibitors. AZT, DDC, DDI and lamuvidine.
2. Non-nucleoside analogue reverse transcriptase inhibitors e.g. Nevirapine
3. HIV Protease inhibitors e.g. Ritonavir, Indivavir. They are the most potent inhibitors of HIV
replication to date.

There are five major types of medicines:

 Reverse transcriptase (RT) inhibitors - interfere with a critical step during the HIV life
cycle and keep the virus from making copies of itself
 Protease inhibitors - interfere with a protein that HIV uses to make infectious viral
particles
 Fusion inhibitors - block the virus from entering the body's cells
 Integrase inhibitors - block an enzyme HIV needs to make copies of itself
 Multidrug combinations - combine two or more different types of drugs into one
These medicines help people with HIV, but they are not perfect. They do not cure HIV/AIDS.
People with HIV infection still have the virus in their bodies. They can still spread HIV to
others through unprotected sex and needle sharing, even when they are taking their
medicines.

Monitoring anti-HIV therapy

1. Viral Load
Initiation - viral load is now the preferred method of monitoring therapy. There should be >=
1 log reduction in viral load, preferably to less than 10,000 copies/ml HIV-RNA within 2-4
weeks after the commencement of treatment. If <0.5 log reduction in viral, or HIV-RNA stays
above 100,000, then the treatment should be adjusted by either adding or switching drugs.
Monitoring - viral load measurement should be repeated every 4-6 months if patient is
clinically stable. If viral load returns to 0.3-0.5 log of pre-treatment levels, then the therapy is
no longer working and should be changed.
2. CD4 count
Initiation - within 2-4 weeks of starting treatment, CD4 count should be increased by at least
30 cells/mm3. If this is not achieved, then the therapy should be changed..
Monitoring - CD4 counts should be obtained every 3-6 months during periods of clinical
stability, and more frequently should symptomatic disease occurs. If CD4 count drops to
baseline (or below 50% of increase from pre-treatment), then the therapy should be changed
As a result of HAART, mortality from HIV has declined continuously in the N. America and
Europe. However, the long term outlook remains uncertain. These drugs are very expensive
and the patient needs to take them for life. Therefore, there is a question of compliance. It
had been suggested that it would take at least 7 to 10 years to eliminate all HIV particles in
an infected person.

5. Conclusion
HAART is a major therapeutic advance in HIV infection but it probably
favours the development of ADs in certain cases. The risk factors for
these ADs and their pathogenic mechanisms must be determined in
prospective studies.
Take-home messages
• Autoimmune diseases occur in HIV-infected people, most often in
a context of good immunological control (except essentially for autoimmune
hemolytic anemia) or during IRIS (vasculitis, sarcoidosis,
thyroid diseases).
• By improving immune status, HAART might favour autoimmune diseases
onset.
• Several autoimmune diseases may allow HIV infection diagnosis at a
stage of moderate immune deficiency (vasculitis, antiphospholipid
syndrome, immune thrombocytopenia).
• When necessary, immunosuppressant treatments may be used in this
context with good tolerance