Biology Reference
In-Depth Information
isolated, followed by the hepatitis A virus (HAV) in 1973. In the
following years viral agents causing disease similar to HAV and HBV,
but negative for tests specific for these viruses, were reported and
named as non-A, non-B (NANB) hepatitis viruses, with distinct post-
transfusion or enteric epidemiology.
2
The agent for post-transfusion
NANB hepatitis was later identified and named as hepatitis C virus.
2
The agent responsible for ET-NANBH was first identified in 1983 as
being responsible for an epidemic in New Delhi, India in 1955 in
which 29,000 people fell ill; its genome was subsequently cloned and
the agent was named hepatitis E virus (HEV).
3
Hepatitis D virus
(HDV), or the delta agent, is a defective RNA virus that infects liver
cells only if already infected by HBV. There are other viruses like
cytomegalovirus, mumps, rubella and yellow fever viruses that infect
the human liver, but are not considered hepatitis viruses since the pri-
mary sites of infection are extrahepatic. More than 500 million peo-
ple worldwide suffer from viral hepatitis. The disease can either be
self-limiting, as in the case of hepatitis A and E, or can persist, as in
the case of hepatitis B and C, leading to cirrhosis and hepatocellular
carcinoma (HCC).
Viruses are obligate intracellular parasites that have co-evolved
with their hosts to permit virus replication without the destruction of
the host cell. The host's first line of defense is through the innate
response that is mediated with the help of leukocytes, monocytes,
macrophages and natural killer cells. This response is nonspecific
where the killer cells destroy the pathogen by phagocytosis and acti-
vation of lysosomes. In addition, induction of the inflammatory
response mediated by cytokines helps in viral clearance by initiating
apoptotic cell death. Adaptive immunity, on the other hand, is anti-
gen-specific and generates immune memory. Components of adaptive
immunity include antigen-specific lymphocytes such as B cells that
produce neutralizing antibodies, and T cells that have helper and
cytolytic effector functions. The critical balance between survival and
death is dependent upon complex signaling events within a host cell.
Thus the outcome of a viral infection is determined by host responses
such as immunity and cell death and the ability of the virus to coun-
teract and modulate these responses. In HAV and HEV infections,
although the virus is able to establish an infection, the host's innate
