Human immunodeficiency virus (HIV) invades human body immune system (helper T cells) thus compromising its protection against infections. Deterioration of body immune system causes acquired immunodeficiency disease syndrome (AIDS) in HIV infection. There are two types of human immunodeficiency virus: HIV type 1 and HIV type 2. HIV type 1 is extremely virulent as compared to HIV type 2 and it is responsible for most of the HIV infections world wide. Human immunodeficiency virus is classified under genus lentivirus, and family retroviridae. Genus lentivirus is one of the virus groups with a long incubation period (Warren 216).
Structurally, human immunodeficiency virus is enveloped, single stranded and a positive sense RNA virus. Human immunodeficiency virus has RNA which is attached to nucleocapsid protein P7. It has several enzymes which include; reverse transcriptase, intergrase, proteases and ribonuclease. Its covering envelope is made up of phospholipids which contain proteins known as Env attached to it. Env proteins are composed of glycoprotein (gp) 120 and 41 which contribute to the virus virulence (Warren 193).
The glycoprotein facilitates attachment and fusion of the virus to human cell membrane. Human immunodeficiency virus RNA genome has the following genes: gag, env, pol, tat, nef, vpr, rev, vif, and vpu (Warren 193). Gag, env and pol genes are important in forming new structural proteins while rev, nef, tat, vif, vpr and vpu control virus virulence, its replication and ability to cause infection. Vif prevents activities of APOBEC3G while vpr stops cell division. CD4 T helper cells, and major histocompatibility class I and II are controlled by nef proteins. Vpu determines the release of newly assembled viruses in to blood circulation from the infected cells. The ability of LTR to switch regulates production of new viruses. Additionally, proteins of host cell or HIV genome can initiate production of new viruses in the body (Warren 221).
Human immunodeficiency virus infects human body macrophages, helper T cells and microglial cells. This occurs after the glycoprotein molecules on the human immunodeficiency virus particle have interacted with the macrophages and CD4 cells through CCR5 and CXCR4 chemokine receptors (Jay141).
There are various ways in which human immunodeficiency virus is transmitted. They include: transmission through blood transfusion. HIV can be passed from donor’s blood to receiver’s blood if donor is not properly screened to detect the infection. Use of blood contaminated equipments like injection needles and blood giving sets during blood transfusion transmit HIV infection. Mother to child transmission is another way in which human immunodeficiency virus is transmitted. This occurs during delivery or breastfeeding. Newborn gets infected when HIV positive mother’s blood enters into the newborn circulation during delivery. To prevent these instances infected mothers are put on antiretroviral drugs during delivery. Additionally, it is recommended that HIV infected mother should deliver through cesarean section in order to minimize chances of infecting the newborn. Breast feeding of newborn by the HIV infected mothers transmit the infection to newborn. HIV infected mothers are advised not to breast feed their babies but alternatively to use formula milk. Sharing of pricking and cutting objects such as needles and blades transmit human immunodeficiency virus. These instances are common among intravenous drug abuser who share injection needles and syringes. Lastly, sexual transmission is the global leading mode in which human immunodeficiency virus is transmitted. Both vaginal and anal sex transmits human immunodeficiency virus (Basv and Parslow 122).
Human immunodeficiency virus replicates in human cell. The virus enters in to macrophage and CD4 helper T cell through adsorption of glycoprotein to surface receptors leading to fusion of virus particle envelope to the host cell membrane. Human immunodeficiency virus capsid is released from the virus particle in to the human cell after glycoprotein (gp) 421 has penetrated human cell membrane. Human immunodeficiency virus RNA and enzymes enter into the human cell. These enzymes are: protease, ribonuclease, reverse transcriptase and intergrase. In the cell nucleus, transcription occurs catalyzed by enzyme transcriptase leading to formation of double stranded DNA from viral RNA genome. Intergrase catalyze integration of the formed DNA into a host chromosome. After integration the DNA is transcribed in to messenger RNA, it then moves from nucleus to cytoplasm where it is translated to regulatory protein tat and pev. Messenger RNA generates gag and Env. After binding to gag protein RNA particle is packaged into new virus then through endoplasmic reticulum it is transported to Golgi complex. In Golgi complex it is cleaved by protease and proceased in to human immunodeficiency virus and released (Warren 199).
Human immunodeficiency virus clinical presentation is grouped into three stages: the acute stage, latency or chronic stage and the late or AIDS stage. The acute stage occurs between second and fourth week after infection. Latency period or chronic stage start after acute stage and last for many years depending on individual’s life style and treatment with antiretroviral drugs. In this latency stage body CD8 helper T cell fight the infection to suppress its progression. Late stage is terminal stage of this HIV infection. At this stage CD4 cell count is below 200 per microlitre. Additionally, in this stage opportunistic infections set in. Clinical presentation severity of human immunodeficiency virus infection depends on the level of CD4 T helper cell count and individual’s level of viral load (Howard and Makadon 121).
Acute stage presents with following symptoms: inflammation of lymph nodes a condition known as lymphadenopathy, increased body temperature (fever), sore throat due to pharyngitis, pain of body muscles, and mouth sores. There no noticeable symptoms in Latency stage. In late stage, cell mediated immunity is lost and body can not protect itself from infections. Patient experience frequent respiratory infections like otitis media, sinusitis and bronchitis. Opportunistic infection sets in due to reduced body immunity. Patient at this stage is prone to infection such as mycobacterium tuberculosis, Candida infection, herpes simplex, lymphomas, cancers, and Kaposi’s sarcoma (Spicer 98).
There are various ways to prevent human immunodeficiency virus. They include: preventing mother to child transmission. Pregnant mothers should be tested for HIV infection on their first visit to antenatal clinic in order to take necessary precautions to prevent newborn from contracting the infection during delivery and breast feeding incase the mother is infected. It is important to educate public on the infection and how to prevent it. Health education should focus on informing people on how to use protection materials like condoms, importance of abstaining from premature sex and maintaining one faithful sex partner. Women infected with HIV should be discouraged from having unwanted pregnancies. Government and relevant authorities should ensure accessibility of protection material and health facilities to all people. Post exposure prophylaxis to people who have been exposed within 72 hours prevents contracting the infection after exposure. In addition, recent researches indicate that circumcision has positive impact on preventing HIV infection (Spicer 140).
Enzyme linked immunosorbent essay (ELISA) test is used to detect antibodies formed against human immunodeficiency virus. Western blot test is used to confirm ELISA test results by detecting antibodies specific to human immunodeficiency virus. Immunofluorescence assay (IFA) test is proved to be 99.5 % accurate in detecting human immunodeficiency virus. ELISA and western blot are done after IFA to confirm the results (Warren 233).
Antiretroviral medications used to reduce severity of HIV infection are classified in to: nucleoside and nucleotide reverse transcriptase inhibitors. This group of drugs include: Abacavir, tenofovir, lamivudine and zidovudine. They prevent reverse transcription through inhibiting transcriptase enzyme. They have similar mode of action as non nucleoside reverse transcriptase inhibitors like efavirenz, etravirine and nevirapine. Protease inhibitors inhibit protease enzyme. They include atazanavir, darunavir, fosamprenavir and ritonavir. Fusion inhibitors like enfuvirtide and maraviroc prevent virus entry to human cell while Intergrase inhibitors like raltegravir inhibit intergrase enzyme (Warren 236).
Many researches on HIV infection cure have been done but in vain. Am optimistic that HIV infection cure can be discovered after considering the following: Producing drugs to counter the fast replication of the human immunodeficiency virus. The current drugs in use suppress the virus in blood and body major organs leaving the other body organs to harbor the virus. Additionally, to cure HIV infection we should develop medication which can prevent the virus and infected cells from mutation. Also, to curb this infection it is important to develop vaccines capable of forming antibodies against the virus after mutation.
Works cited
Basv, Nagoba and Parslow. Clinical microbiology. New Delhi: B.I publishers, 2009. Print.
Howard, Libman and Harvey Makadon. HIV. 2nd ed. New York: Philadelphia, 2007. Print.
Jay, Levy. HIV and pathogenesis of AIDS. Washington DC: ASM press, 2007. Print.
Spicer John. Clinical microbiology and infectious disease: an illustrated color text. 2nd ed. New York: Churchill Livingstone Edinburgh, 2008. Print.
Warren, Levinson. Review of medical microbiology and immunology. 9th ed. New York: McGraw-Hill, 2006. Print.