Category Archives: Controversy

Did vaccine introduce HIV? or was it the monkey hunter?

HIV causes immunodeficiency diseases (AIDS). The first case was reported in 1959 in Congo. However, the cure, prevention, and its exact origin remained to be hand-waving. There had been hypotheses regarding the origin circulating within our scientific community. One of them is the administration of polio vaccine introduced by a virologist Hilary Koprowski. The administration of the polio vaccine in Congo coincided with the place and the time of the initial case of HIV. This hypothesis is commonly known as the oral polio vaccine theory. The other hypothesis, which is agreed by most scientists, is the cut hunter hypothesis.

Polio vaccine is an attenuated vaccine, which a chemical reagent, formaldehyde, was added to a pool of poliovirus to kill the virus. But before killing the virus, scientists need to obtain the pool of polioviruses. In order to produce virus, the cultivation procedure is dependent on monkey kidney cells. In the 1960s, polyomavirus SV40 was found to be integrated in the genome of monkey kidney cells. Like papillomavirus, polyomavirus SV40 can induce S phase progression. As a result of SV40 genome integration, cells can grow without control. Consequently, malignant tumor is developed in the host organism. Because monkey kidney cells are used to cultivate poliovirus, the researchers then asked if the polio vaccine contains any SV40 genome. The answer was yes. This finding put anyone who received the oral polio vaccination from 1955 to 1963 at risk for cancers.

Related Article: Papillomavirus causes cervical cancer.

So how does this have anything to do with the debate on the origin of HIV? HIV is classified under the family of lentiviruses. HIV is a virus that contains a dimer of positive strand RNA. After entering the cell, HIV reverse transcribes RNA into double stranded DNA. With an enzyme called integrase, the HIV double stranded DNA is integrated into the host genome. As SV40 is found inside the monkey kidney cells, scientists speculated that the polio vaccine contains SIV (the monkey version of HIV). It is a good hypothesis, as HIV and SIV DNAs can be integrated into our genome (as provirus). This hypothesis is known as the oral polio vaccine hypothesis. However, the SIV genome was not found in any stocks of polio vaccines. With this piece of information, the oral polio vaccine theory was discarded.

The other hypothesis, which everyone believes in, is the cut hunter hypothesis. This hypothesis believes that a hunter in Congo who had a cut when butchering a chimpanzee. This results in a cross-species transmission of SIV, and leads to the HIV-1 epidemic that circulates worldwide.

A visit to the current controversy: manmade mutant H5N1 influenza virus (2)

From the last issue, a current controversy about the mutant H5N1 was discussed. I will continue the discussion by talking about some essential aspects of deriving successful mutants. These mutants can have completely different tropism for tissues or animals. The understanding by how a mutant is derived had recently stirred a debate between academic freedom and bioterrorism. Personally, I think the understanding of how to derive mutants is crucial in aiding us to define how new viruses are evolved.

Receptor influences viral entry

Binding to the cellular receptor is the first step when the virus comes in contact with the host cell. The cells that express a particular type of receptor make them susceptible to viral infection. Other than the susceptibility, one must also consider if cells have the required machinery for a productive infectious cycle. This is what defined the term, permissive. Here, I will discuss a paper from Higgs’ lab at the University of Texas, called a single mutation in Chikungunya (CHIKV) virus affects vector specificity and epidemic potential (shown right).

The CHIKV strain that circulates in 2005-2006 epidemic on Reunion island is different from normal CHIKV infection. This particular strain is not transmitted through the normal route: Aedes aegypti (which is the same species responsible for dengue viral infection in human). In fact, it is transmitted by the Asian tiger mosquito called Ae. albopictus. By sequencing, these researchers found a particular mutation at the E1 protein at the site 226 (mutated from Alanine to Valine).

Interestingly, when they look at the replication of both strains within the same organism, they found that the 226V mutant is more successful in replicating within the Ae. albopictus but not at the Ae. aegypti.

They also supported this result by looking at the dissemination of each strain. It is clear that the 226V mutant is more successful in completing the infectious cycle against 226A mutant only in Ae. albopictus. In contrast, 226V mutant does not have an advantage in Ae. aegypti. The researchers then went on to support the conclusion by infecting animals with the mosquitoes.

E1 is a part of the spike on the CHIKV envelope. Complexed with E2 in the hetero-trimeric spike structure, this complex facilitates the interaction with cellular receptor, entry, and budding. The mutation in E1 protein can completely change the tropism for its vector. It is also able to compete against wildtype viruses. The bottom line is the change in viral envelope proteins can change its preference of cells that it can infect. In other words, envelope proteins must be mutated in a way that it can recognize cells that express different receptors.


PLoS Pathog. 2007 Dec;3(12):e201.

A single mutation in chikungunya virus affects vector specificity and epidemic potential.

Tsetsarkin KA, Vanlandingham DL, McGee CE, Higgs S.

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A visit to the current controversy: manmade mutant H5N1 influenza virus (1)

A researcher, named Ron Fouchier, claimed that he has created a new variant (or you may call it the mutant) of H5N1 influenza virus. Normally, H5N1 influenza virus can not be transmitted between human and human. And it rarely transmits from an avian source to human. But when it does, the fatality rate is approximately 50%. Dr. Fouchier, who is an investigator at the Erasmus Medical Center in the Netherlands, claimed that he has created a new and airborne H5N1 influenza virus. This mutant is transmissible between mammals. Although his research finding is yet published and opened to the public, his research has created a controversy in the balance of academic freedom and protecting the nation from bioterrorism. As a member of the general public, I, too, have no idea what the introduced mutation Dr. Fouchier made to the original H5N1 strain. As a nascent virologist here at UC, here I will make some speculation and discuss about the ongoing situation.

Redefining the risk of mutant virus

One of the key aspects circulating in the news is the fact that this mutant is “airborne”. In my opinion, almost all viruses that disseminate within the respiratory tract are airborne. If viruses are able to replicate in our lung, it is highly possible that the mucus or droplets from an infected individual contain a considerable amount of viruses. The reason why some viruses is not able to disseminate effectively is possibly due to the failure to replicate efficiently within the host, resulting in a low concentration/titer of viruses which may not be enough to infect another susceptible individual.

“TONY EASTLEY: Scientists who have produced an airborne mutated of the killer bird flu virus H5N1 say it’s essential their research be published, but opponents say the biosecurity risks are too high and would be a “how to” manual for terrorists.” ABC NEWS

The public is now informed that this mutant virus is airborne. But honestly, the concern should be focus on the fact that it has now adapted to be spread between human and human. In the past, humans are the accidental host of H5N1 viruses. In other words, it is rare when the H5N1 viruses infect humans. So the concern should focus on the fact that the specific mutation can change the targeting species and disseminating efficiency. For an effective virus replication cycle, the virus must find a susceptible host cell that expresses a certain protein on its membrane. These proteins are known as receptors. These receptors are the key for the virus to recognize the proper cells to enter. The next barrier the virus needs to overcome is whether the host cells can provide the necessary factors for it to replicate.

In the next issue, we will continue to discuss how the viral surface proteins can be mutated to recognize different hosts (which I think it’s one of the key barriers to derive a new species in viruses). We will go over some current literature on CHIKV mutation and how the mutation on the viral surface protein can change the selectivity and the replication efficiency.


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