The spread and persistence of influenza viruses in normal and cyclophosphamide‐treated mice

Abstract

The persistence and extrapulmonary spread of three strains of influenza virus, the mouse neuro-adapted A/NWS virus, the wild-type strain A/Victoria/75, and a recombinant virus RIT4050, bearing surface antigens derived from A/Victoria/75, were studied in both normal and cyclophosphamide-treated CBA mice following either intranasal or intracerebral inoculation. All three viruses showed increased lethality in mice in the presence of cyclophosphamide but exhibited distinctive patterns of replication and spread. The recombinant virus RIT4050 showed a reduced ability to replicate, persist, and spread in CBA mice compared to either A/NWS or A/Victoria/75 viruses, and in general, the A/NWS virus persisted to a greater extent than the A/Victoria/75 virus in both normal and treated mice. However, in the presence of cyclophosphamide, no extrapulmonary spread of A/NWS virus was observed. The reasons for the differences are discussed.

Carrot Pomace Polysaccharide (CPP) Improves Influenza Vaccine Efficacy in Immunosuppressed Mice via Dendritic Cell Activation

“…Given that CPP may stimulate the anti-viral activity of the innate immune system, we were interested in the humoral immune response to an influenza vaccine challenge. Consistent with previous literature [25,26], vaccine-specific antibody titers were almost abolished in cyclophosphamide-injected animals given a quadrivalent inactivated influenza vaccine (Figure 4). Remarkably, treatment with CPP significantly recovered the total IgG response to a level comparable to that of GTP.…”

Dynamics of viral growth, viral enzymatic activity, and antigenicity in murine lungs during the course of influenza pneumonia

“…Immunosuppressive treatment with cyclophosphamide interferred with the elimination of infectious virus and neuraminidase activity but did not lead to a significant (P < 0.05) increase in viral antigen concentrations as compared to nontreated animals. These observations are consistent with the reported impairment to antiviral defenses associated with cyclophosphamide treatment [ 1,8]. The failure to detect an increasing accumulation of total viral antigen (independent of viability) may indicate dissemination of virus to extrapulmonary locations [5] or an as yet undefined mechanism.…”