The CCR5-Δ32 Allele: A Natural Resistance to HIV Virus Human immunodeficiency virus, most commonly known as HIV, is an acquired virus that attacks the immune system of the host and eventually leads to acquired immunodeficiency syndrome otherwise known as AIDS. HIV is a relatively new disease in human populations, AIDS was first observed in homosexual males in 1981 (Herron et al., 2014, p. 2). Later, in 1983, soon after the discovery of AIDS, scientists identified HIV virus as being responsible for AIDS, we now know that AIDS is the last stage of HIV infection (Tortora et al., 2013, p. 545). Since then HIV virus has been wrecking havoc in present day populations across the world. Since its discovery in the early 1980’s it has been estimated
…show more content…
It is important to note that on the envelope surface are small glycoprotein spikes, which help the HIV virus to attach to its target (Tortora et al., 2013, p. 545). HIV virus mainly affects CD4+ T helper cells and monocytes but can affect any cell that has CD4 receptors on their surface (Galvani and Novembre, 2005). Once in an individuals system the HIV virus seeks out its target cells, usually CD4+ T helper cells, and using its glycoprotein spikes attaches to the CD4 receptors on the T helper cell surface. While attaching to the CD4 receptors the glycoproteins spikes also attach to chemokine coreceptors on the T helper cell surface, most commonly this coreceptor is CCR5. This process is known as attachment. After attachment the viral and host membrane fuse, a process known as fusion, and then the viral contents are emptied into the host cell, a process known as entry. After entry the HIV virus transcribes its RNA into DNA and integrates its DNA into the host cells chromosome. From this point the virus may lay dormant in a period of latency or it may signal for the production of new viruses to continue infecting other T helper cells (Tortora et al., 2013, p. 545-547). Currently there is no cure for HIV but with the advent of new drugs it has become a chronic infection that infected …show more content…
Initially it was thought that the black plague most likely would have provided this selective pressure. This was disproven when Mecsas and colleagues performed tests on mice to see if the CCR5-Δ32 allele provided protection against Yersinia pestis, the causative agent of the plague. Mecsas and colleagues found that the CCR5-Δ32 allele did not provide the mice any protection from Yersinia pestis disproving the hypothesis that the plague could have provided the strong selective pressure scientists were looking for (Mecsas et al., 2004). Further testing by Galvani and Saltkin using mathematical models to predict whether the plague or small pox provided the selective pressure showed that small pox was more likely the culprit. Galvani and Saltkin hypothesized this was due to the fact that small pox affects small children which takes away more chances at reproduction versus an adult who had been infected with the plague who has had chances to reproduce (Galvani and Saltkin,
It is important to note that on the envelope surface are small glycoprotein spikes, which help the HIV virus to attach to its target (Tortora et al., 2013, p. 545). HIV virus mainly affects CD4+ T helper cells and monocytes but can affect any cell that has CD4 receptors on their surface (Galvani and Novembre, 2005). Once in an individuals system the HIV virus seeks out its target cells, usually CD4+ T helper cells, and using its glycoprotein spikes attaches to the CD4 receptors on the T helper cell surface. While attaching to the CD4 receptors the glycoproteins spikes also attach to chemokine coreceptors on the T helper cell surface, most commonly this coreceptor is CCR5. This process is known as attachment. After attachment the viral and host membrane fuse, a process known as fusion, and then the viral contents are emptied into the host cell, a process known as entry. After entry the HIV virus transcribes its RNA into DNA and integrates its DNA into the host cells chromosome. From this point the virus may lay dormant in a period of latency or it may signal for the production of new viruses to continue infecting other T helper cells (Tortora et al., 2013, p. 545-547). Currently there is no cure for HIV but with the advent of new drugs it has become a chronic infection that infected …show more content…
Initially it was thought that the black plague most likely would have provided this selective pressure. This was disproven when Mecsas and colleagues performed tests on mice to see if the CCR5-Δ32 allele provided protection against Yersinia pestis, the causative agent of the plague. Mecsas and colleagues found that the CCR5-Δ32 allele did not provide the mice any protection from Yersinia pestis disproving the hypothesis that the plague could have provided the strong selective pressure scientists were looking for (Mecsas et al., 2004). Further testing by Galvani and Saltkin using mathematical models to predict whether the plague or small pox provided the selective pressure showed that small pox was more likely the culprit. Galvani and Saltkin hypothesized this was due to the fact that small pox affects small children which takes away more chances at reproduction versus an adult who had been infected with the plague who has had chances to reproduce (Galvani and Saltkin,