FLAVIVIRUS: IMMUNE RESPONSE AND HOST
DEFENSES
Many individuals living in flavivirus endemic areas develop
subclinical infection in childhood and gain a degree of protective
immunity. Visitors to these areas who first come into contact with
arboviruses as adults often die from flavivirus infection since they lack
immunity.
Some arboviruses, such as dengue, can produce a wide
range of symptoms in infected individuals. Depending on the
immune response and host defenses, dengue infection may produce inapparent
disease, an undifferentiated respiratory illness, dengue fever or dengue
hemorrhagic fever/dengue shock syndrome.
Infection with a particular flavivirus, dengue, is
associated with a particular phenomenon known as "immune enhancement". In
the case of dengue, maternally or naturally acquired antibodies
against one serotype do not prevent against infection with another
serotype. In fact previous exposure to one
strain may exacerbate disease caused by exposure to a second strain. The
four distinct dengue serotypes are cross-reacting, but not
cross-neutralizing. Upon reinfection, the body responds to the first
strain with which it was infected and mounts a strong immune
response. Uptake of the virus by macrophage cells increases and
severe disease (dengue hemorrhagic fever or dengue shock
sydrome) may result. This phenomenom is specific to dengue and is known as
"immune enhancement".
Hepatitis C induces persistent infection and high antibody titers in
the chronically infected. Immune responses are unable to clear HCV from
the body since most of the virus is bound in virus-antibody complexes.
Thus the viral genome remains for years in the liver cells producing a
chronic carrier state. But HCV does not overpower the immune system in all
cases since the case fatality rate from fulminant hepatitis is less than
1%. The exact nature of the antibody response is unknown because extensive
studies have not yet been conducted on the immune response to HCV.