Breakdown of the blood--cerebrospinal fluid barrier to immunoglobulin in mice injected intracerebrally with a neurotropic influenza A virus. Post-exposure treatment with monoclonal antibody promotes recovery.

Mice may be protected from the invariably fatal consequences of intracerebral (i.c.) inoculation of A/WSN influnza virus by intravenous injection with 0.5 mg of virus-specific monoclonal anti-hemagglutinin antibody given 2 days after i.c. challenge. The integrity of the blood-cerebrospinal fluid (CSF) barrier in such mice has been examined by comparing specific immunoglobulin (Ig) titers in serum and CSF. It seems that the process of virus growth results directly in substantial breakdown of the blood-CSF barrier at some time between 63 and 96 h after i.c. exposure to virus. The exogenously administered, virus-specific monoclonal antibody is not obviously involved either in abrogating the integrity of this physiological barrier system or in promoting inflammation. In fact, higher Ig titers are found in CSF for an antibody that does not bind to the virus. This presumably reflects the fact tht virus-infected cells in the central nervous system are adsorbing specific Ig from the CSF.