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A major obstacle to the success of oncolytic viruses is the patient immune system which naturally attempts to deactivate any virus. This can be a particular problem for intravenous injection, where the virus must first survive interactions with the blood complement and neutralising antibodies. [42]
Another major challenge with using oncolytic viruses as therapy is avoiding the host's natural immune system which will prevent the virus from infecting the tumor cells. [7] [8] Once the oncolytic virus is introduced to the host system, a healthy host's immune system will naturally try to fight off the virus. Because of this, if less virus is ...
Other viruses utilize host cell proteins to shield viral DNA until it has reached the nucleus. Upon entry into the host cell cytoplasm, the HIV-1 capsid is recognized and bound by cyclophilin A (CypA); this affinity interaction stabilizes the capsid and prevents exposure of the HIV-1 cDNA to pattern recognition receptors in the cytoplasm.
Finally, the host restriction for human viruses makes it unethical to experimentally transmit a suspected cancer virus. Other measures, such as A. B. Hill's criteria, [10] are more relevant to cancer virology but also have some limitations in determining causality. Simplified diagram of the structure of the Epstein–Barr virus (EBV).
Of the many different viruses being explored for oncolytic potential, an adenovirus was the first to be approved by a regulatory agency, the genetically modified H101 strain. It gained regulatory approval in 2005 from China's State Food and Drug Administration (SFDA) for the treatment of head and neck cancer. [2] [3]
When the virus replicates faster than the immune system can control, it can destroy cells and harm the body, and it can even incite an over-zealous immune reaction that can cause other damage.
For infections to occur, the virus has to hijack host factors and evade the host immune response for efficient replication. Viral replication frequently requires complex interactions between the virus and host factors that may result in deleterious effects in the host, which confers the virus its pathogenicity. [5]
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