RAMEZ ALBAB

With a cure perhaps unattainable, eradication of HIV/AIDS in the same way as smallpox (with no cure) was eliminated, may be the most feasible option. According to Dr. Brian Williams of the South African Centre for Epidemiological Modelling and Analysis, eradication of HIV/AIDS is an achievable goal that could be attained by 2050 if the current HIV/AIDS research paradigm is changed from focus on finding a cure to stopping transmission.

Since the onset of the HIV/AIDS pandemic in 1981 cases of people with a natural immunity to HIV have been documented. Although these persons, called long-term non-progressors (LTNPs) are infected with HIV, they never develop AIDS. When LTNPs are infected, some suffer an initial drop in their T-4 (CD4) cell count. However, when their T-4 (CD4) cell count reaches around 500 it stabilizes and never drops again preventing the onset of AIDS. Furthermore, while CD8+ T-Cells (even in large numbers) are ineffective against HIV-infected T-4 (CD4) cells in progressors (persons without a natural immunity to HIV), the National Institutes of Health (NIH) reported in a December 4, 2008 press release that "CD8+ T-Cells taken from LTNPs [can efficiently] kill HIV-infected cells in less than [an] hour" in which "a protein, perforin (produced only in negligible amounts in progressors), manufactured by their CD8+ T-Cells punches holes in the infected cells" enabling a second protein, "granzyme B" to penetrate and kill them.


Per Genetic HIV Resistance Deciphered (Med-Tech, 7 January 2005) the roots of this immunity dates back a thousand years due to "a pair of mutated genes - one in each chromosome - that prevent their immune cells from developing [Chemokine (C-C motif) receptor 5 (CCR5) receptors] that let [HIV penetrate]." This mutation likely evolved to provide added protection against smallpox according to Alison Galvani, professor of epidemiology at Yale University. Based on the latest scientific evidence, the mutated CCR5 gene (also called delta 32 because of the absence or deletion of 32 amino acids from its cytokine receptor) located in Th2 cells, developed in Scandinavia and progressed southward to central Asia as the Vikings expanded their influence. Consequently up to 1% of Northern Europeans (with Swedes being in the majority) followed by a similar percentage of Central Asians have this mutation, which if inherited from both parents provides them total immunity while another 10-15% of Northern Europeans and Central Asians having inherited the mutation from one parent exhibit greater resistance in lieu of complete immunity to HIV.

At the same time, even though the CCR5 mutation is absent in Africans, a small also exhibit percentage natural immunity (possibly developed through exposure) to HIV/AIDS - CD8+ T-Cell generation that effectively kills HIV-infected cells and mutated human leukocyte group A (HLA) antigens that coat the surface of their T-4 (CD4) cells to prevent HIV from penetrating based on an intensive study of 25 Nairobi prostitutes who per The Amazing Cases of People with Natural Immunity against HIV (Softpedia, 27 June 2007) have "had sex with hundreds, perhaps thousands of HIV-positive clients" and shown no sign of contracting HIV.

In addition, people with larger numbers of the CCL3L1 gene that produces cytokines (proteins that "gum" up CCR5 receptors) to prevent HIV from entering their T-4 (CD4) cells, per Genetic HIV Resistance Deciphered have greater resistance to HIV in comparison to others within their ethnic group that possess lesser quantities of the CCL3L1 gene and get "sick as much as 2.6 times faster."

At the same time, up to 75% of newborn babies also possess natural immunity (for reasons still not known) when exposed to HIV-positive blood. Although born with HIV antibodies - thus HIV-positive, newborns "usually lose HIV antibodies acquired from their HIV-positive mothers within 12-16 - maximum 18 months," in which their "spontaneous loss of [HIV] antibodies" without medical intervention is called seroreversion. "However, with the exception of very few instances, these infants are not HIV-infected" conclusive proof of a natural immunity to HIV.[1] Furthermore, when pregnant HIV-positive women are administered highly active antiretroviral therapy (HAART), which lowers the viral concentration of HIV in their blood, an astonishing 97% of their newborns lose their HIV antibodies through seroreversion to become HIV-free per the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) as posted under Surveillance Monitoring for ART Toxicities Study in HIV-Uninfected Children Born to HIV-Infected Mothers (SMARTT) (Clinical Trials.gov, 29 March 2008). However, at this time, it is not known if these newborns retain their natural immunity throughout their lives.

HIV is spherical in shape and approximately 120 nanometers (nm) in diameter (or 60 times smaller than a red blood cell). It is composed of two copies of single-stranded convoluted RNA surrounded by a conical capsid and lipid membrane that prevents antibodies from binding to it. HIV also consists of glycoprotein (gp120 and gp41) spikes and is a highly mutating virus. Its genome changes by as much as 1% each year, significantly faster than "killer" cytotoxic T-Cells (CD8+) can adapt. It is transmitted through bodily fluids.

Human immunodeficiency virus (HIV), the retrovirus responsible for acquired immune deficiency syndrome (AIDS) has been around since between 1884 and 1924 (while lentiviruses, the genus to which HIV belongs, have existed for over 14 million years) when it entered the human population from a chimpanzee in southeastern Cameroon during a period of rapid urbanization. At the time, no one noticed nor knew that it would result in one of the deadliest pandemics. Nor was anyone aware that some would possess a natural immunity, a cure would remain elusive a decade into the 21st century, and a significant number of deceased victims would be purged from mortality statistics distorting the pandemic's severity.


As the number of cases spread from Cameroon to neighboring countries, namely the Democratic Republic of Congo (DRC), Gabon, Equatorial Guinea, and the Central African Republic, they drew little attention even as victims died in scattered numbers from a series of complications (e.g. Pneumocystis pneumonia (PCP), Kaposi's sarcoma, etc.) later attributed to AIDS. This was likely because of Africa's limited interaction with the developed world until the widespread use of air travel, the isolated, low incidence of cases, HIV's long incubation period (up to 10 years) before the onset of AIDS, and the absence of technology, reliable testing methods and knowledge surrounding the virus. The earliest confirmed case based on ZR59, a blood sample taken from a patient in Kinshasha, DRC dates back to 1959.

The outbreak of AIDS finally gained attention on June 5, 1981 after the U.S. Centers for Disease Control (CDC) detected a cluster of deaths from PCP in Los Angeles and New York City. By August 1982, as the incidence of cases spread, the CDC referred to the outbreak as AIDS. The responsible retrovirus, HIV, was isolated nearly a year later (May 1983) by researchers from the Pasteur Institute in France and given its official name in May 1986 by the International Committee on Taxonomy of Viruses. During this period, HIV-related mortality rates rose steadily in the United States peaking in 1994-1995.