Present study outlines a comprehensive view of published information about the underlying mechanisms operational for progression of chronic hepatitis C virus (HCV) infection to development of hepatocellular carcinoma (HCC). These reports are based on the results of animal experiments and human based studies. Although, the exact delineated mechanism is not yet established, there are evidences available to emphasize the involvement of HCV induced chronic inflammation, oxidative stress, insulin resistance, endoplasmic reticulum stress, hepato steatosis and liver fibrosis in the progression of HCV chronic disease to HCC. Persistent infection with replicating HCV not only initiates several liver alterations but also creates an environment for development of liver cancer. Various studies have reported that HCV acts both directly as well as indirectly in promoting this process. Whereas HCV related proteins, like HCV core, E1, E2, NS3 and NS5A, modulate signal pathways dysregulating cell cycle and cell metabolism, the chronic infection produces similar changes in an indirect way. HCV is an RNA virus and does not integrate with host genome and therefore, HCV induced hepatocarcinogenesis pursues a totally different mechanism causing imbalance between suppressors and proto-oncogenes and genomic integrity. However, the exact mechanism of HCC inducement still needs a full understanding of various steps involved in this process.

Hepatitis E virus infection (HEV) is a major cause of acute viral hepatitis in the developing world. The immunopathology of HEV infections has not yet been elucidated. The virus is noncytopathic, and therefore, liver injury may be attributed to immune-mediated damage by cytotoxic T cells and natural killer cells. Therefore, we studied the nature of immune cells involved in HEV-induced liver damage using immunohistochemistry in liver biopsies taken from patients with HEV-induced acute liver failure and demonstrated a significant infiltration of activated CD8(+) T cells containing granzymes. These findings suggest the possible involvement of cytotoxic T cells in disease pathogenesis during HEV infection.

Neuromodulation is an important treatment modality for a variety of pelvic floor disorders. Percutaneous tibial nerve stimulation (PTNS) and sacral neuromodulation (SNM) are currently the two approved methods for delivering this therapy. Percutaneous tibial nerve stimulation is a minimally invasive office-based procedure that has shown efficacy in the treatment of overactive bladder, fecal incontinence, and pelvic pain. It has the advantage of minimal side effects but is limited by the need for patients to make weekly office visits to receive the series of treatments. Sacral neuromodulation uses an implanted device that stimulates the S3 nerve root and can improve symptoms of overactive bladder, non-obstructive urinary retention, fecal incontinence, and pelvic pain. This paper will review the most recent literature regarding this topic and discuss their advantages and limitations and recent innovations in their use.

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