Abstract
Acute RNA viral encephalomyelitis is a serious complication of numerous virus infections. Antibodies in the cerebral spinal fluid (CSF) are correlated to better outcomes, and there is substantive evidence of antibody secreting cells (ASCs) entering the central nervous system (CNS) and contributing to resolution of infection. Here, we review the RNA viruses known to cause acute viral encephalomyelitis with mechanisms of control that require antibody or ASCs. We compile the cytokines, chemokines, and surface receptors associated with ASC recruitment to the CNS after infection and compare known antibody-mediated mechanisms as well as potential noncytolytic mechanisms for virus control. These non-canonical functions of antibodies may be employed in the CNS to protect precious non-renewable neurons. Understanding the immune-specialized zone of the CNS is essential for the development of effective treatments for acute encephalomyelitis caused by RNA viruses.
Highlights
Encephalomyelitis is a dangerous presentation of numerous viral infections with potentially devastating long-term neurological sequelae
A majority of what is known about this mechanism comes from studies of the Sindbis virus (SINV), rabies virus (RABV), West Nile virus (WNV), and murine hepatitis virus (MHV) in mice and is summarized here
In the case of MHV strain JHM mouse hepatitis virus (JHMV), many of the chemokines, cytokines, and surface markers are similar to those expressed during SINV infection and support the concept of a shared process for antibody secreting cells (ASCs) recruitment and accumulation in the central nervous system (CNS) (Table 2) [54]
Summary
Encephalomyelitis (inflammation of the brain and spinal cord) is a dangerous presentation of numerous viral infections with potentially devastating long-term neurological sequelae. Infection with most encephalomyelitis-causing viruses more often results in asymptomatic or mild febrile illness without neurologic disease This is in part due to the rapidly mounted innate and adaptive immune responses to prevent the virus’s entry into the central nervous system (CNS). As this pathology can be caused by numerous viruses, there is considerable variability in mortality, ranging from
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