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The response to treatment is measured by sustained viral response (SVR), defined as the absence of detectable RNA of the hepatitis C virus in blood serum for at least 24 weeks after discontinuing treatment, [112] and rapid virological response (RVR), defined as undetectable levels achieved within four weeks of treatment. Successful treatment ...
Viral hepatitis is liver inflammation due to a viral infection. [ 1 ] [ 2 ] It may present in acute form as a recent infection with relatively rapid onset, or in chronic form, typically progressing from a long-lasting asymptomatic condition up to a decompensated hepatic disease and hepatocellular carcinoma (HCC).
The best way to reduce the long-term risk of HCC is to achieve sustained virological response (SVR). [111] SVR is defined as an undetectable viral load at 12 weeks after treatment completion and indicates a cure. [112] [113] Currently available treatments include indirect and direct acting antiviral drugs.
Viral load is often expressed as viral particles, (virions) or infectious particles per mL depending on the type of assay. A higher viral burden, titre, or viral load often correlates with the severity of an active viral infection. The quantity of virus per mL can be calculated by estimating the live amount of virus in an involved fluid.
A count of the viral load is routine before the start of HIV treatment. [1] If the treatment is not changed, then viral load is monitored with testing every 3–4 months to confirm a stable low viral load. [1] Patients who are medically stable and who have low viral load for two years may get viral load counts every 6 months instead of 3. [1]
Prognosis varies between people, and both the CD4 count and viral load are useful for predicted outcomes. [32] Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. [6] After the diagnosis of AIDS, if treatment is not available, survival ranges between 6 and 19 months.
Certain viruses, such as human cytomegalovirus (HCMV) and hepatitis C (HCV), have adapted to suppress the function of MAVS in the antiviral innate immune response, aiding in viral replication. [7] [11] HCMV impairs MAVS through the viral mitochondria-localized inhibitor of apoptosis protein (vMIA), thus reducing the pro-inflammatory cytokine ...
Viral disease is the sum of the effects of viral replication on the host and the host's subsequent immune response against the virus. [3] Viruses are able to initiate infection, disperse throughout the body, and replicate due to specific virulence factors. [2] There are several factors that affect pathogenesis.