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Until the beginning of the 21st century scientists around the world dominantly presumed that a polio vaccine, used in Africa during the late 1950s, was responsible for introducing the primate precursor, Simian Immunodeficiency Virus (SIV), to humans. The assumption was that kidneys of SIV infected chimpanzees may have been used for the preparation of this oral polio vaccination. The initiation of pandemic AIDS disease through a vaccine against the polio virus, especially dangerous for children, would have meant a real tragedy. However, in 2001 studies proved that this vaccine samples from the 1950s exhibited no traces of SIV. Although the polio vaccine theory has been refuted, there are still a few of countries in Africa where this view is still present. This fact causes a problem by preventing the complete extinction of the polio virus.
This essay will give an insight into the state of research regarding the transmission of the precursor virus to humans, the spread of HIV and the origin of AIDS. Such investigations could hopefully lead to new rudiments of therapeutic ways to treat HIV and AIDS in the future.
Origin of HIV
In 1981, AIDS was recognized for the first time but it brought up the question, how long has the virus already existed in the human population? Worobey et al. (2008) addressed this interrogation by comparing the two oldest known sequences of HIV-1 group M viruses. Both their characterized viral sequence of a lymph node biopsy sample from 1960, DRC60, and the sequence of a blood plasma sample from 1959, ZR59 (Zhu et al., 1998), were collected in Kinshasa, capital of the Democratic Republic of Congo. Old viral sequences are good markers for the early spread of HIV because viral RNA shows a high rate of evolution so that considerable sequence changes occur in a couple of decades (Korber et al. 2000). The significant genetic deviation between DRC60 and ZR59, of about 12%, indicates that diversification of HIV-1group M occurred a long time before the first recognition of AIDS and before obtaining the oldest known viral sequences. Worobey (2008) and his team used statistical methods, as relaxed molecular clock analysis, to estimate the date for a common progenitor of HIV-1 group M strains.Thus they could extrapolate the date of an ancestor between 1902 and 1921.
Furthermore, the biggest variety of group M strains has recently been found in Kinshasa (Vidal et al., 2000), which points to the assumption that most of the early diversification took place in Kinshasa and around.
There are known two HIV subspecies, HIV-1 and HIV-2. HIV-2 is less virulent and confined to West Africa. In contrast, HIV-1 is highly infectious and distributed globally. Furthermore, HIV-1 strains can be divided into 4 groups: N, O and P are quite rare and restricted to Cameroon and surrounding countries, whereas the major group M causes about 95% of all HIV infections worldwide.
All these types derived independently from SIVÂ´s of non-human primates by zoonotic transmissions. It is established that HIV-2 originates from sooty mangabeys (Hahn et al., 2000) which live on the west coast of Africa from Senegal to Ghana. The following part of this essay, however, will concentrate on HIV-1. In 1989, a closely related virus was found in two captive chimpanzees (Peeters et al., 1989; Huet et al., 1990). But in the next years only a few additional viral samples could be found in wild-living apes. Due to this, SIV seemed to be very rare in chimpanzees and they were not acknowledged as the natural origin of human AIDS pandemic. A reason for that lack of SIV in chimpanzees could be the way of achieving samples. Until then it was only possible to gain SIV samples by invasive methods like isolating from blood or tissues. Thereby, this constituted a very restricting factor because chimpanzees are highly threatened and live in isolated jungle territories. But in recent years some new non-invasive methods were developed allowing to study and to follow chimpanzees meticulously in their natural habitat. Keele et al. (2006) conducted a epidemiological field study with the increase of molecular aspects in the southeast of Cameroon. They collected fecal and urine from the forest floor applying for genetic fingerprinting and SIV specific antibody detection. This facilitates to identify the species, gender and immune status of each individual. By using such non-invasive methods it was possible to show that SIV infections are quite usual in wild-living chimpanzees. Moreover, they were able to describe SIV strains that are closely related to the groups M and N of HIV-1. Thus, this study indicates chimpanzees in Cameroon as the probable natural reservoir of HIV-1 groups M and N, whereas the source of group O remains uncertain. The more recently discovered group P likely derived from gorillas (Plantier et al., 2009).
So far, this essay discussed the reservoir of HIV but how did the transmission occur? The mostly accepted explanation for this chimpanzee-to-human transmission would be the contact of humans with the blood of animals during hunting and butchering for bushmeat (Wolfe et al., 2004). Hunting of wild animals has been, and is even nowadays, still very common in west and central Africa. As a consequence, some other questions arose: Why did the HIV pandemic start in Kinshasa and not until beginning of the twentieth century? The source of HIV-1 has been traced to chimpanzees in the southeast of Cameroon (Keele et al., 2006) whereas the early spread and diversification of HIV occurred further south in Kinshasa (Worobey et al., 2008). Moreover, many people were hunting for bushmeat before twentieth century. Thus, the opportunities for such zoonotic transmissions were existent for a long time. The solution could be that HIV was in want to a high total population to propagate and AIDS to become an epidemic disease. It therefore seems likely that only the rapid growth of cities and conurbations in the beginning of the twentieth century ensured the establishment and early spread of HIV-1 (Worobey et al., 2008). Kinshasa has been one of such growing cities and is furthermore located at the Congo River. At this time, waterways have been the mainlines of communication and transportation so that the virus could reach Kinshasa via rivers flowing further south from the southeast of Cameroon finally joining the Congo River (Paul M. Sharp and Beatrice H. Hahn, 2008). In the developing Kinshasa sexual contacts increased and the first red-light districts with prostitution emerged so that HIV could spread out widely (McNeil, 2010). An additional crucial event for the strong propagation of HIV could have been the introduction of millions of syringes into Africa in the 1950s for campaigns to wipe out smallpox, polio or malaria. These syringes were often re-used and facilitated the virus to spread out (McNeil, 2010).
Origin of AIDS
Humans acquired SIV from chimpanzees, their closest living relatives. But do chimpanzees represent the origin of SIV? Is SIV of chimpanzees (SIVcpz) pathogenic or is AIDS a new feature restricted to HIV? It has been widely supposed that SIV only causes small sickness in chimpanzees and seems to be non-pathogenic as in sooty mangabeys and in almost the other 40 monkey species harboring SIV. Until Keele et al. (2009) could demonstrate the opposite. They showed that groups of wild chimpanzees, who were naturally infected with SIV, developed hallmarks of AIDS and had a 10- to 16- fold higher mortality rate than uninfected animals. This indicates that SIVcpz induces immune deficiency by mechanisms that are quite analogical to those of HIV-1. Thus, AIDS is not a new characteristic of human AIDS. However, differences exist regarding the pathogenicity and the course of disease. The researchers assume that SIVcpz is more pathogenic than HIV-2 or SIV of sooty mangabeys but less pathogenic than HIV-1 (Keele et al., 2009). This points to the assumption that the pathogenicity correlates with the time a species is harboring this virus.
However, if SIV is pathogenic in chimpanzees, they must have received SIV more recently so that they could not adapt as well as monkeys. Genome analysis confirmed this by revealing that the SIVcpz genome exhibits a mosaic structure of regions from different SIV lineages. Nowadays it is probable that this recombinant virus derived from lentiviruses of the red-capped mangabey and one or more lineages of the greater spot-nosed monkey (Bailes et al., 2003).
As it is known, conventional immunization therapies are not able to protect against HIV and progression to AIDS. The currently available antiretroviral therapeutics only have the ability to delay the progression to AIDS, but cannot stop it. Consequently, there have to be found new rudiments for therapeutic ways to treat HIV. An opportunity could be the investigation of the origin and evolution of HIV and SIV so that comparisons may provide insights into viral and host factors, which are responsible for HIV and SIV pathogenicity and disease progression. The research has made a significant progress in this field in the last 10 years, as suggested in this essay. Natural SIV infections are non-pathogenic and seem to be an evolutionary coadaption leading to a amicable coexistence (Sodora, 2009). Nevertheless, they share certain resemblances with pathogenic infections in humans and chimpanzees. So far, researchers assumed that natural SIV hosts generate a strong adaptive immune response to control virus replication completely but recent studies showed that they are also unable. As traditional AIDS vaccine research based on this premise to reduce virus replication with a strong immune response, a new paradigm in AIDS research is required (Sodora, 2009). Differences between pathogenic HIV or SIV and natural SIV infections merely appear in the chronic phase regarding the level of immune activation. Active immune downmodulatory mechanisms, as the downregulation of CD4+ T-cells, seem to be responsible for the course of harmless SIV infections (Sodora, 2009).
In conclusion it is to say that further investigations are required to compare HIV infections with non-pathogenic SIV infections in monkeys. In future, the AIDS-research could hopefully learn from such evolutionary adaptations to prevent the progression to AIDS. Furthermore, more studies are necessary to contrast disease-causing mechanisms in such congeneric species, like humans and chimpanzees, to identify relevant pathogenic factors of HIV and SIV.
This are promising new approaches for developing an AIDS vaccine, but still time and basic research are required to understand and to imitate mechanisms which have evolved over long time of evolution.