In a surprising move, the research team at Penn State, part of the Homeland Security Initiative Office of Military and Security Programs, has published a medical article about a key mechanism that is operative in Parainfluenza Virus-5 (PIV-5) replication [1].

According to the Journal of Virology, the article provides scientists with a critically important piece of the puzzle regarding viral replication associated with PIV-5 infection. The journal authors report that PIV-5 relies on a specific host protein, known as Akt1, for its viral protein synthesis and replication. These researchers had found that the deployment of specific Akt inhibitor compounds acted to reduce the replication of PIV-5. In fact, the group had reported that viral titers had been reduced over one-thousand fold. However, this effect did depend on the cell-line used for their in-vitro experiments.

The NCF has found some preliminary information about Akt1. Among some of its properties: Akt1 is a protein kinase that is also considered to be an oncogene. [A protein kinase is a kinase enzyme that modifies other proteins by chemically adding phosphate groups to them (i.e. - phosphorylation). An oncogene is a gene that is capable of causing the transformation of normal cells into cancer cells.] Akt1 appears to mediate insulin's actions and is involved in the signal transduction of growth factors such as insulin growth factor-1 [2]. Akt1 has been found to impact cell survival and development [3]. Alterations to Akt1 may lead to a greater susceptibility to genotoxic stress and apoptosis [4]. In addition, Akt1 is amplified in gastric cancers [5] and upregulated in breast cancers. In fact, a recently published paper indicates that Akt1 governs breast cancer progression in-vivo [6]. Furthermore, Akt plays a role in thyroid cancer [7] aswell as prostate cancer [8].

Somehow, the NCF gets the impression that we may be just scratching the surface hereas PIV-5 may be involved in and perhaps be responsible for cancer development. This isn't too far fetched considering that PIV-5 is capable of generating a persistent infection resulting in immune evasion and dramatic alteration to the host's immune system. The NCF is optimistic since this latest information provides us with a new target for potential antiviral drug intervention. Future research, by the NCF, will hopefully be aimed in this direction. It is worth noting that antiviral therapy may prove to be just an initial first step towards viral antagonism since other immune-mediated mechanisms may be at play here. These additional factors may subsequently be found
to be critical to the immune reconstitution efforts that may be required to ultimately clear this infection from the host.

Reference: