1
Currently, alpha interferon is the only recognized therapy for chronic viral hepatitis.
2
Host genes that regulate systemic inflammation upon chronic viral infection are incompletely understood.
3
Hepatitis C virus (HCV) is a major cause of chronic viral hepatitis.
4
Cytotoxic T-lymphocytes are critical in the clearance of chronic viral infections such as HTLV-1.
5
Inhibitory receptors play a crucial role in regulating CD8 T-cell function during chronic viral infection.
6
Dysfunction of CD8+ T cells can lead to the development of chronic viral infection.
7
Treatment of this chronic viral infection has considerably improved with the introduction of ribavirin-interferon combination therapy.
8
Conclusion: Routine clinical ultrasound is a not a sensitive predictor of early fibrosis in chronic viral hepatitis.
9
Exhaustion of CD8(+) T cells severely impedes the adaptive immune response to chronic viral infections.
10
Immune responses induced during the early stages of chronic viral infections are thought to influence disease outcome.
11
T cell exhaustion during chronic viral infection is well described, but effects on antibody-mediated effector activity are unclear.
12
Exhausted T cells express multiple co-inhibitory molecules that impair their function and limit immunity to chronic viral infection.
13
Such hepatic expansion of the CTL population controlled chronic viral infection of the liver after vaccination with DNA.
14
Persistent signaling by these receptors during chronic viral infection sculpts the transcriptional regulatory programs of virus-specific T cells.
15
Interpretation: Several simple, inexpensive operational interventions can substantially improve engagement and retention along the chronic viral hepatitis care continuum.
16
Conclusion: HGDN should be considered a precancerous lesion when it appears during follow-up of chronic viral hepatitis or cirrhosis.
