Human immunodeficiency virus is the causative agent of acquired immunodeficiency syndrome (AIDS) in humans. There are two variants of HIV that causes AIDS in humans viz: HIV-1 and HIV-2. While HIV-1 is mainly transmitted from mother to child and is thus a neonatal infection acquired congenitally, HIV-2 is transmitted via blood and sexual contact or having unprotected sex with an already infected person. HIV was first discovered as a human viral pathogen in the early 1980’s; and the disease (i.e. AIDS) has since caused innumerable number of morbidity and mortality in the human population. The actual origin of AIDS in the human population is as a result of cross-species infection of humans by a chimpanzee Lentivirus particularly the simian immunodeficiency virus (SIV), which infects only monkeys, chimpanzees and like primates in the west central African region. The scourge of the AIDS disease has impacted negatively on the economies of the world due to its ability to deteriorate the immune system of HIV-infected individuals.


HIV is mainly transmitted via sexual intercourse especially unprotected sexual intercourse with an infected person. Transmission via contact with blood and other sharp objects contaminated with blood of an HIV-positive individual is also possible. HIV can also be transmitted congenitally from an infected mother to an unborn child. Intravenous drug users, heterosexuals and homosexuals are also at high risk of infection with HIV. HIV is entirely an infection of the immune system of humans, and the CD4 T helper cells (TH) of the cellular immune system are the main receptor of the virus. HIV binds to the CD4 cells and also on other cellular cells of the human host that bears the CD4 marker on their surfaces. This binding leads to the suppression of the individual’s cellular immune response due to the loss of CD4 T helper cells.

The CD4 T helper cells are unique in the cellular immune response of humans in that they play a central role in both cellular and humoral immune response when foreign bodies (i.e. antigens inclusive of pathogenic viruses like HIV) invades the body. CD4 cells secrete numerous cytokines that activates other specific components of the immune system such as the macrophages; delayed-type hypersensitivity T cells (TDTH) and the cytotoxic T cells (CD8) which carries out the killing of antigens in the body. HIV infects and kills immune system cells (especially the CD4 lymphocytes) that are vital for effective immune response against pathogens that invades the body. Once the HIV has attached to the CD4 cells, it facilitates its entry into the cell through several cell-entry techniques. And once inside the cell, the virus uncoats and its RNA genome is transcribed with the help of its reverse transcriptase (RT) to a viral DNA or provirus that is integrated into the chromosomal DNA of the host cell. Since the CD 4 cells are primarily responsible for the mediation or activation of T cell immunity during antigen invasion of the body, acquired immunodeficiency syndrome (AIDS) finally results following a marked decrease or suppression of the CD4 cells of the affected individual by HIV.

HIV infection can be acute (during which the infection is rapid in progression) or chronic (which the infection is slow in progression) in occurrence but the actual clinical outcome of the disease is dependent on several factors which include the genetics of the infecting virus, the genetics of the affected host, the virulence of the infected virus and the immune status of the host. HIV-infected people remain infectious throughout the period of their lifetime especially in the acute stage of the disease, and such individuals are potential routes via which the disease can be transmitted to susceptible populations. At the acute stage of HIV infection, the viral load in infected individuals is very high and such patients show a high level of viraemia at this phase when viral count of their blood is taken. During the chronic stage of the disease, some of the dead CD4 cells are rapidly replaced and the patients usually show low viral load count and normal CD4 cell count too.

But AIDS definitely sets in; and it is generally characterized by the emergence of several opportunistic infections caused by bacterial, fungal and protozoal pathogens and even some viruses such as cytomegalovirus (CMV). Development of tumours (especially cancers of the skin) and some neurological disorders such as wasting and aseptic meningitis are other accompanying (opportunistic) infections that characterize AIDS in HIV-infected individuals. These opportunistic infections exemplify the main clinical features of AIDS in HIV infected individuals and they appear during the progressive loss of CD4 cells in infected persons. Unexplained weight loss, fever, pharyngitis, headache, arthralgia, myalgias, and malaise are some of the main non-specific symptoms or clinical features that characterize the primary stage of HIV infection (i.e. the stage at which the individual is newly infected).

The incubation period of the disease is usually 2-6 weeks after exposure but this can also last up to 3 months or 6 months. It is noteworthy that the course of HIV infection in humans varies from one individual to another. While some individuals can show clinical signs of AIDS within 10 years of infections, others can live beyond this limit without showing any clinical signs of AIDS. However, the AIDS stage of HIV infection is usually defined by a marked decrease in the CD4 level of the infected host. A CD4 cell count of less than 200 cells/µL is clinically indicative of AIDS stage. The appearance of some opportunistic infections, cancers or tumours can also define the AIDS-stage of the disease. AIDS usually appear after about 10 years of infection with HIV; and due to the marked disintegration of the host immune system especially that of the cellular immunity, the individual is exposed to plethora of opportunistic infections caused by other microbes including bacteria, viruses, protozoa and fungi as aforementioned. The severity of HIV infection according to studies have been linked to co-infection with other non-retroviral agents such as hepatitis B virus (HBV), hepatitis C virus (HCV) and CMV amongst others; and this has affected or increased the rate of progression of the disease in HIV-positive patients who have these co-infections.


Clinically, the presence of opportunistic infections such as cryptococcal meningitis and recurrent vulvovaginal candidiasis amongst others mentioned above without a known cause of immunodeficiency in a person should raise suspicion of HIV infection. Nevertheless, the laboratory diagnosis of HIV infection is largely dependent on the detection of HIV-1 or HIV-2 antibodies in the serum or blood samples of patients using serological or molecular techniques that includes enzyme linked immunosorbent assay (ELISA), polymerase chain reaction (PCR) and other rapid diagnostic laboratory techniques. In addition, specific antigens of the virus especially the capsid proteins of HIV such as p24 can be detected in serum following infection using HIV antigen detection kits. The detection of HIV capsid proteins some days after infection aids in the early diagnosis of infection since these proteins appear in the serum or blood of infected individuals few days after infection and before HIV-1 or 2 antibodies starts to appear. The AIDS defining illness of the disease can also be confirmed in the laboratory by determining the patients CD4 count. And if the CD4 cell count is less than 200 cells/µL, then the individual is in the AIDS phase of the disease.


One of the major impediments to the effective treatment of HIV infection is the development of resistance to some readily available antiviral drugs especially when such drugs are used singly for treatment. Aside this, the development and preservation of latent HIV-1 in some cellular and anatomical sites of HIV-1 infected individuals has contributed a great deal to the inability of current antiretroviral therapy (ART) to eradicate the virus from the body of people living with the disease. These immunological and pharmacological privileged sites of the body such as lymph nodes are known as reservoir sites; and they are important sanctuaries where transcriptionally silent but replication competent latent HIV-1 are hiding in the body of people living with HIV/AIDS (PLHA).

More so, upon the discontinuation of ART, the reservoir sites of latent HIV-1 in PLHA continue to serve as repertoire and source via which the general circulation is replenished with the infectious virus. This has made curing and eradication of HIV-1 difficult. Which is why researchers are actively looking out for chemicals known as latency reversing agents (LRAs) that can purge the reservoir sites, and thus flush out the latent HIV-1 from their hiding places in the body of PLHA. In lieu of this, antiviral drugs are now administered in combinations of three antivirals i.e. as a triplet; and this has helped to contain the possibility of development of resistance to antiretroviral drugs when they are used singly. To this end, highly active antiretroviral therapy (HAART) which is the type of HIV treatment in which antiviral drugs are used in combination as triple therapy is now being used for HIV treatment. In HAART, one nucleoside analog and one protease inhibitor are included in the antiretroviral therapy, and the main aim of this triple therapy is to slow the development of resistance to any of the agent and also to ensure effective treatment.

Most antiretroviral drugs target key steps in the replication cycle of retroviruses in order to inhibit or slow their replication. Also, antiretroviral drugs help to reduce the number of viruses in the individual as quick as possible so that the nefarious activity of the virus (especially in suppressing the cellular immunity) can be contained and assuaged. The major classes of antiretroviral drugs available for the treatment of HIV-infection are nucleoside inhibitors and protease synthesis inhibitors. The nucleoside inhibitors include zidovudine or azidothymidine (AZT), lamivudine (3TC) and didanosine (ddl). These antiviral drugs are nucleoside analogs and they basically inhibit the activities of reverse transcriptase (RT) during HIV replication. They bind to the active site of RT, and thus becomes incorporated into the growing DNA strands (i.e. the viral DNA).

By interfering with the synthesis of viral DNA, AZT acts as chain termination to stop the elongation of the DNA strand so that an incomplete genome of the virus will be produced. Protease inhibitors basically act by inhibiting the production of protease which is vital for the formation of viral proteins. Examples of antiviral agents that are protease inhibitors include ritonavir (RTV), indinavir (IDV) and saquinavir (SQV). Protease inhibitors generally inhibit viral maturation since proteases play critical roles in the synthesis of viral proteins required for the coupling of new virions.

No effective vaccine currently exist for the vaccination of susceptible human population against HIV infection but vaccine development for HIV prevention is still underway and putative. The AIDS virus (HIV) has a rapid rate of maturation or replication, and its genetics is inconsistent due to the ease with which the virus mutates into different and new forms. And the human body can still not produce protective immunoglobulins against HIV. These factors have greatly affected the development of novel and potent vaccine for the effective vaccination of the human race against the scourge. Having safe sex and sticking to only one partner when married, screening of blood and organs before transfusion or transplantation and avoiding the sharing of sharp objects such as needles are some of the measures that can be taken for the prevention of HIV infection.


Acheson N.H (2011). Fundamentals of Molecular Virology. Second edition. John Wiley and Sons Limited, West Sussex, United Kingdom.

Ahmad K (2002). Norwalk-like virus attacks troops in Afghanistan. Lancet Infect Dis, 2:391.

Alan J. Cann (2005). Principles of Molecular Virology. 4th edition. Elsevier Academic Press,   Burlington, MA, USA.

Alba R, Bosch A and Chillon M (2005). Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther, Suppl 12:S18-S27.

Alberts B, Bray D, Johnson A, Lewis J, Raff M, Roberts K and Walter P (1998). Essential Cell Biology: An Introduction to the Molecular Biology of the Cell. Third edition. Garland Publishing Inc., New York.

Balows A, Hausler W, Herrmann K.L, Isenberg H.D and Shadomy H.J (1991). Manual of clinical microbiology. 5th ed. American Society of Microbiology Press, USA.

Barrett   J.T (1998).  Microbiology and Immunology Concepts.  Philadelphia,   PA: Lippincott-Raven Publishers. USA.

Balfour H. H (1999). Antiviral drugs. N Engl J Med, 340, 1255–1268.

Balfour H.H Jr (1999). Antiviral drugs. N Engl J Med; 340:1255–1268.

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