Prognosis

B virus exposure may or may not lead to infection, but B virus infection almost always results in disease in humans, which usually occurs within 1 month of exposure.[2][4] How the disease progresses depends on several factors, including the site of infection and the amount of virus transmitted during infection. In the absence of intervention, human infection typically progresses from localised signs or non-specific flu-like symptoms to neurological symptoms as the virus infects the central nervous system (CNS).[4] Neurological symptoms may be gradual or abrupt in onset.[4] Encephalomyelitis develops as the virus infects the CNS, and the usual outcome is death, which is often attributed to respiratory failure due to ascending paralysis.[37] The mortality rate with B virus infection is approximately 80% in untreated humans. The mortality rate is reduced if aggressive antiviral treatment is instituted in a timely manner; it has been estimated that 80% of patients survive when treatment with intravenous acyclovir or ganciclovir is initiated promptly.[10]

Based on what is known about the pathophysiology of B virus infection and reasoning by analogy from other alphaherpesvirus infection, those who survive B virus disease are presumed to remain latently infected. However, recurrence of symptoms is rare; only two reports of presumed clinical recurrence of pre-existing B virus infection exist.[18][38] Many survivors do suffer lifelong moderate-to-severe neurological sequelae, sometimes requiring institutionalisation.[32] The virus is presumed to persist in the peripheral nervous system (usually the nerve ganglia) for the lifetime of the host; it is not present in blood or serum of infected hosts. The virus can be detected in other body fluids (vesicular lesions, cerebrospinal fluid, oral and genital secretions) during symptomatic illness and continuing for a duration while on antiviral therapy. For this reason, active viral shedding should be demonstrated to have stopped before intravenous antivirals are discontinued. Many physicians have advised a transition from intravenous antiviral therapy to ongoing oral valaciclovir or aciclovir maintenance therapy after symptoms and active virus shedding have been documented to have stopped.[4] However, there is a lack of good data on when or whether treatment should be discontinued; therefore, this should be done with expert consultation.[4] Long-term monitoring of recovered patients should include some plan for periodic monitoring to confirm that virus shedding has not reactivated. At least one case of B virus infection has presented similarly to ocular zoster, in which the person who was reported not to have had contact with macaque monkeys for many decades was interpreted as a late clinical presentation of a long-term silent B virus infection.[18] Recurrent ocular B virus disease has also been described in a patient treated with valaciclovir.[38]

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