What is HIV AIDS?
HIV is a retrovirus that causes AIDS. HIV attacks the immune system. This system consists of cells and organs that protect the body against diseases like infections and cancer. HIV attacks the immune system through special types of white blood cell known as CD4cells. CD4 cells play an important role in orchestrating and controlling the functions of the whole immune system.
Once HIV is in the immune system, it multiplies inside the CD4 cells, disabling and killing them in the course of the infection, and thus interfering with their normal function. The immune system gradually deteriorates until it reaches a point where it can no longer fight off any infection.
The infected person frequently gets infections and even some forms of cancer which a healthy immune system would have gotten rid of quite easily. These infections are known as opportunistic infections. HIV infection, once established, cannot be eliminated by the body or by drugs.
Statistics on HIV AIDS
According to the 2006 report on the Global AIDS Epidemic by the Joint United Nations Programme, approximately 37.2 million adults and 2.3 million children were living with HIV at the end of 2006. During 2006, some 4.3 million people became infected with HIV, and approximately 2.9 million deaths resulted from HIV/AIDS.
By 30 June 2006, 25,703 people in Australia were infected with HIV, 9,827 had AIDS and 6,621 died as a result of HIV/AIDS. NSW had the highest number of deaths, followed by Vic, QLD, WA, SA, ACT, NT and TAS.
Risk Factors for HIV AIDS
HIV can be transmitted through the following routes:
- Unprotected sexual intercourse with an infected partner
- Contact with infected blood through blood transfusion, sharing needles or syringes contaminated with infected blood by injecting drug users
- Mother to child transmission (vertical transmission) during pregnancy, at birth and breastfeeding
Progression of HIV AIDS
Throughout the disease, viral load steadily increases and immunodeficiency progressively worsens (due to the decreasing CD4 count), thereby causing HIV/AIDS to manifest in stages. The World Health Organization (WHO) has categorized HIV disease into 4 stages:
- Stage I (also known as primary HIV infection): In this stage, the person has no symptoms whatsoever and may not be aware they are infected.
- Stage II (also known as clinically asymptomatic stage): This stage may last for 8-10 years with no major symptoms except for swollen glands (lymph nodes), some weight loss, mouth ulceration and mild skin and nail infections.
- Stage III (also known as symptomatic HIV infection): By this stage, the immune system is significantly affected and the infected person now begins to manifest many symptoms, such as severe weight loss, chronic diarrhoea, persistant fever, tuberculosis, severe bacterial infections (e.g. pneumonia and meningitis).
- Stage IV (also known as AIDS): The immune system is now severely damaged and the symptoms become even more severe. The person is now severely wasted, has severe recurrent bacterial infections, develops cancers such as Kaposi sarcoma, and other infections like Pneumocystis carinii pneumonia (PCP), toxoplasmosis and HIV encephalopathy.
Symptoms of HIV AIDS
The presentation of HIV depends on the stage of the disease that the patient is in. In the early stages of the disease there may be few or no (mild) infections, while in the later stages there may be more severe infections and even some forms of cancer.
Clinical Examination of HIV AIDS
On examination, the following may be found:
- Weight loss
- Lung infections such as pneumonia or tuberculosis
- Fungal nail infections
- Bacterial infections (i.e. infections of muscles, bones, joints, brain coverings)
- Kaposi’s sarcoma
- CNS disease (i.e. encephalopathy)
How is HIV AIDS Diagnosed?
- Full blood count: This is a test to check on the levels of white blood cells, red blood cells, platelets and haemoglobins in your blood. This test needs to be done before and regularly after treatment to check for anaemia (reduced blood haemoglobin) and reduction of other blood cells.
- Urea and electrolytes: These are chemical compounds normally found in blood. Their levels are controlled by the renal system. This test is done to check on the condition of the kidneys. If the kidneys are functioning normally, then the levels of urea and creatinine will be normal. Otherwise the levels will be elevated.
- Hepatitis B and C testing: HIV patients are at high risk of hepatitis B and C infections, which are also contacted through blood.
Prognosis of HIV AIDS
It takes about 8 to 10 years from initial infection and symptom manifestation to the development of AIDS. Once AIDS has developed, untreated disease results in death in about 20 months. Treatment with HAART can prolong life and delay disease progression, and improve quality of life.
HIV AIDS Prevention
Protection during intercourse (condoms), blood screening, disposable instruments.
For birth: prophylaxis and consider caesarean section, formula feeding.
How is HIV AIDS Treated?
Treatment of infected patient
- Aim is to stop virus spread permanently.
- Monitor blood viral load and CD4 count.
- Start antiretrovirals early before immunodeficiency sets in.
- Use 3 antiretrovirals (2 nucleoside analogue reverse transcriptase inhibitors and a protease inhibitor).
- Change to a new combination if viral load rebounds.
HIV AIDS References
- NIH. National Institute of health, U.S. Department of Health and Human Services: How HIV causes AIDS; 2004 [cited 2007 Feb 26]. Available from: www.niaid.nih.gov/factsheets/howhiv.htm.
- Kumar P, Clark M. Clinical Medicine: WB Saunders; 2002.
- Scosyrev E. An overview of the Human Immunodeficiency Virus featuring Laboratory Testing for Drug Resistance. Clinical laboratory Science 2006 [cited FALL 2006]; 19(4): 23-1245.
- UNAIDS. AIDS epidemic update: special report on HIV/AIDS: December 2006; 2006. Available
- NCHECR. Australian HIV Surveillance Report: The HIV epidemic in Australia. In: National Centre in HIV Epidemiology and Clinical Research; 2006.
- Bean P. New Drug targets for HIV. Clinical Infectious Diseases 2005;41 ( Suppl 1).