Friday, December 14, 2007

Natural immunity to HIV

Since the outbreak of HIV, there have been the occasional noted case where an individual after repeated exposure to HIV did not acquire the infection. This is more than simply good luck. Researchers have been gathering evidence to explain this percieved natural immunity to HIV. This understanding will drastically improve the accuracy and effectiveness of treatment by individualizing drug regime and therapies. And of course hopefully lead to the developement of a vaccine.
Recent studies have proposed that the basis of HIV immunity is due to our ethnicity and history of disease experienced by our ancestors. These factors effect our genetic code and determine whether we will be susceptible to the HIV infection.
Genetic resistance to HIV infection works in a variety of ways between different ethnic groups. A genetic defect in those with European or Central Asian ancestry provide the most successful resistance to HIV as yet identified. Around 1% of Northern Europeans are virtually immune to HIV with Swedish people being most likely to remain uninfected. These highly HIV resistant individuals all possess a pair of mutated genes (1 per chromosome) that prevent the developement of the CCR5 cellular receptor that the HIV virus uses to infiltrate the cell. This genetric trait msut be inherited from both parents to have the most effect (homozygous). Inheriting the mutated gene from one parent provides some resistance but it is comparatively weaker (heterozygous). 10 -15% of Northern Europeans have this lesser immunity. By using molecular clocks, this genetic mutation dates back to the middle ages.
Other ethnic groups possess lesser HIV resistance due to increased copies of the gene CCL3L1.
Individuals with the greatest number of copies of CCL3L1 (as compared with their ethnic group)
had increased immunity to HIV. Those with the lowest numbers were the most susceptible and became ill approximately 2.5 times faster than others who were also infected. Increased copies of CCL3L1 appear to effect the amount of cytokines released during the inflammatory response. the cytokines attach to cellular receptors and guide the immune cells. The more cytokines that are attached to cellular receptors means less available sites for HIV infiltration. This type of immunity is not nearly as complete as the genetic mutation of CCR5 but is more prevalent in populations.
The genetic mutations that provide HIV resistance originate before its emergence. The question is why would a mutation persist for so long without reason? Many researchers beleive that other diseases, such as the bubonic plague, dysentary, or small pox were the stimulant to maintain a protective gene. This genetic protection would increase the survival of generations versus individual short term.
Although genetic induced HIV resistance is incredibly promising for the developement of a vaccine and impoved therapies, it does not replace the vital protection of safe sex. There is no guarenteed immunity only better odds.

References:

Novembre, J., Galvani, A., Slatkin, & Montgomery. (2005). The genetic spread of CCNR5 ^ 32 HIV-resistant allele. PLoS Biology, Vol. 3 (11), 1954.

Dotinga, R. (2005). Genetic HIV resistance Deciphered. Retrieved December 14, 2007, from
http://www.wired.com/medtech/health/news/2005/01/66198

2 comments:

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