Who is immune to aids

Scientists have known for some time that these individuals carry a genetic mutation known as CCR5-delta 32 that prevents the virus from entering the cells of the immune system but have been unable to account for the high levels of the gene in Scandinavia and relatively low levels in areas bordering the Mediterranean. They have also been puzzled by the fact that HIV emerged only recently and could not have played a role in raising the frequency of the mutation to the high levels found in some Europeans today.

Some scientists have suggested this disease could have been smallpox or even bubonic plague but bubonic plague is a bacterial disease rather than a virus and is not blocked by the CCR5-delta 32 mutation. Around , historians spread the idea that the plagues of Europe were not a directly infectious disease but were outbreaks of bubonic plague, overturning an accepted belief that had stood for years.

Professor Duncan and Dr Scott illustrated in their book, Return of the Black Death , Wiley , that this idea was incorrect and the plagues of Europe were in fact a continuing series of epidemics of a lethal, viral, haemorrhagic fever that used the CCR5 as an entry port into the immune system.

Maturation occurs either in the forming buds or after budding from the host cell The mature virions are able to infect another host cell. Innate immune cells e. Tissue macrophages are one of the target cells for HIV. These macrophages harbour the virus and are known to be the source of viral proteins. However, the infected macrophages are shown to lose their ability to ingest and kill foreign microbes and present antigen to T cells.

This could have a major contribution in overall immune dysfunction caused by HIV infection. Dendritic cells DCs. DCs are large cells with dendritic cytoplasmic extensions. These cells present processed antigens to T lymphocytes in lymph nodes. These cells transport HIV from the site of infection to lymphoid tissue. The follicular DCs, found in lymphoid tissue, are also key antigen-presenting cells that trap and present antigens on their cell surfaces.

In the lymph node follicles, DCs provide signals for the activation of B lymphocytes. Natural killer NK cells. NK cells have lytic activity against cells that have diminished expression of m ajor h istocompatibility c omplex MHC I antigens.

Scientists suspect that its commonness comes from being spared by deadly plagues in the distant past. However, there is disagreement over which disease or diseases influenced the mutation over time. Much research has shown that the mutation may have given some people immunity to the waves of bubonic plague that swept through Europe during the 12th through 15th centuries. But University of Berkeley researchers suggest smallpox is a likely cause for the mutation's spread.

In a report in the Proceedings of the National Academies of Science, the scientists explained that smallpox was around far longer than the plague and killed far more people. And smallpox especially affected younger children, who were not yet old enough to reproduce. An estimated 10 percent to 15 percent of those descended from Northern Europeans have the lesser protection.

Using formulas that estimate how long genetic mutations have been around, researchers have discovered that the mutation dates to the Middle Ages. Similar research in mitochondrial DNA -- passed along by women -- has suggested that Europeans are all descended from seven Ice Age matriarchs.

Why would the mutation stick around so long instead of giving up the ghost? Researchers initially thought the mutation provided protection against the bubonic plague that caused the Black Death in Europe.

Those with the mutation would have lived longer and had more children while many of their neighbors died off. The fact that the genetic mutation also provided protection against HIV centuries later would just be a coincidence.

The plague scenario has been largely discarded in favor of another deadly scourge. According to Galvani, while the plague came and went, smallpox stuck around well into the 20th century, providing even more incentive for a protective gene to live on: It would keep people alive generation after generation, instead of just during one brief epidemic. There are other cases of genetic mutations affecting two diseases: People who inherit one of the two mutations necessary to develop sickle-cell anemia end up with extra resistance to malaria, said Dr.

Last February, Mosier co-wrote a report in the journal Nature that debunked the plague theory after researchers found that mice bred with the AIDS-protective gene mutation still got sick with the plague.