Abstract
Chronic inflammation is recognized as a threat factor for cancer progression. Release of inflammatory molecules generates microenvironment which is highly favorable for development of tumor, cancer progression and metastasis. In cases of latent viral infections, generation of such a microenvironment is one of the major predisposing factors related to virus mediated tumorigenesis. Among various inflammatory mediators implicated in pathological process associated with cancer, the cyclooxygenase (COX) and its downstream effector molecules are of greater significance. Though the role of infectious agents in causing inflammation leading to transformation of cells has been more or less well established, however, the mechanism by which inflammation in itself modulates the events in life cycle of infectious agent is not very much clear. This is specifically important for gammaherpesviruses infections where viral life cycle is characterized by prolonged periods of latency when the virus remains hidden, immunologically undetectable and expresses only a very limited set of genes. Therefore, it is important to understand the mechanisms for role of inflammation in virus life cycle and tumorigenesis. This review is an attempt to summarize the latest findings highlighting the significance of COX-2 and its downstream signaling effectors role in life cycle events of gammaherpesviruses leading to progression of cancer.
Highlights
Subsequent to primary infection, gammaherpesviruses follow two distinct life cycles in the human host: a latent infection in which the virus persists in a dormant state for long periods of host’s life, and a lytic form which results in release of infectious virions capable of de novo infection important for spread of virus to new hosts
The over-expression of COX-2 is a constant factor in Kaposi’s sarcoma associated Herpesvirus (KSHV) positive BC-3 cell lines (Paul et al, 2011). These findings suggest critical role for COX-2 mediated inflammatory pathway in Epstein Barr Virus (EBV) and KSHV mediated pathogenesis (Paul et al, 2013c)
The study demonstrated that both prostaglandin E2 (PGE2) and COX-2 regulated inflammation associated processes by modulating secretion of cytokine and controlled KSHV latency which is essential for viral genome maintenance and survival of host cell (SharmaWalia et al, 2010b)
Summary
Subsequent to primary infection, gammaherpesviruses follow two distinct life cycles in the human host: a latent infection in which the virus persists in a dormant state for long periods of host’s life, and a lytic form which results in release of infectious virions capable of de novo infection important for spread of virus to new hosts. Extensive studies have been done to understand the biological importance of the upregulated COX-2 level and subsequent increased level of PGE2 molecule and over-expression of EP receptors in development of malignancies associated EBV and KSHV (Paul et al, 2013c).
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