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Related post: challenge by wild-type virus. It appears that the properties of attenuation, genetic stability in vivo , and protective efficacy of ts-1 NG-1 and ^-1 NG-16 make both mutants promising vaccine candidates. 23-60 ZOl AI 00175-03 LID 2) Immunosuppressive effect of serum antibody on response of cotton rats to live RS virus administered intramuscularly (IM) Since an RS virus vaccine is most urgently needed during the first few months of life, the issue of immunosuppression by maternally derived serum antibody represents a potential obstacle to successful immunization in this age group. Work reported last year showed that cotton rats born to mothers which had previously been infected with RS virus were refractory to intramuscular (IM) vaccination with live wild-type virus. In contrast, animals born to mothers without prior exposure to RS virus were successfully vaccinated by the IM route. Although specific immune factors were responsible for the immunosuppressive effect, the nature of these factors, and the amount necessary to block immunization were not determined. We examined the phenomenon of immunosuppression in greater detail by administering pooled cotton rat RS virus antisera intraperitoneal ly (IP) to seronegative animals which were than immunized IM with live wild-type virus. Those animals which were given antisera were unable to respond to the IM vaccine, whereas the animals which received pooled control sera (free of RS virus antibody) prior to vaccination were successfully immunized. This demonstrated that serum antibody or a concomitant serum immune factor, could produce immunosuppression. A second experiment, designed to determine the dilution endpoint of serum blocking factors required for immunosuppression, showed that pooled antisera diluted 1:256 was sufficient to completely block IM vaccination, although this amount of antisera did not yield detectable neutralizing antibody in the serum of recipient rats. This suggests that a live virus vaccine administered IM may not be useful in individuals most in need of immunoprophylaxis, since the greatest impact of RS virus occurs during the first six months of life when most infants possess maternally derived, serum neutralizing antibody for RS virus. The immunosuppressive effect of antibody on parenteral RS virus vaccination raises the possibility of a similar effect during immunization with a live attenuated virus administered into the respiratory tract. To study this possibility, we inoculated seronegative cotton rats IP with the pooled antisera described previously, then administered live, attenuated RS virus (ts-1 NG-16) intranasal ly (IN) the following day. Following challenge with wild type virus (three weeks later) all the animals Lithobid 300 Mg were shown to be resistant to challenge (IN) with wild type virus, whether they had received immune or control (antibody-free) sera prior to vaccination. It would appear that the immunosuppressive effect seen in IM vaccination is not seen during IN vaccination, and that topically applied RS virus vaccines may confer effective immunity independent of antibody in serum at the time of vaccination. 23-61 ZOl AI • 00175-03 LID 3) Assessment of Structural Alterations and Antigenic Patterns of RS Infections Immunohi stoarcheol ogy - Using the enzyme-linked immunohistologic technology developed in this laboratory, and pathologic specimens derived from culture proven cases of RS virus infection obtained from collaborators, it was possible to define a constellation of histologic changes accompanying fatal RS virus disease. Previously unrecognized endobronchial lesions were detected which include a lytic focal endobronchial mucosal dissolution which leaves small characteristic mucosal ulcerations. This focal lytic endobronchitis is unique in that there is a paucity of responding leukocytes despite a large amount of viral antigen and tissue destruction. These Lithobid 300 changes are likely the precursor lesions to the changes recognized by Zinserling which in his studies could not be definitely linked to RS virus. Involvement of the peribronchial mixed mucous and serous glands by RS virus has not been described previously. Immunochemical staining revealed viral antigen in such tissues. Of interest, the lungs of infants or elderly individuals who died of RS virus disease revealed minimal structural alteration of the acinar tissues despite distinct viral inclusion bodies and the presence of as much viral antigen as is seen in tissue culture cells after 96 hours of experimental infection. The physiologic consequences of viral replication in the mucus glands are not known but may contribute to a decreased efficiency of the local pulmonary defense mechanisms and perhaps contribute to the bronchiolar plugging observed in RS virus disease. These observations suggest that RS virus may have an effect on the function of large areas of the lung not actually infected by the virus. Although recognized as responsible for the development of endobronchial syncytial giant cells since the work of Adams, RS virus has not been considered a Buy Lithobid cause of giant cell pneumonia. Analysis of fatal RS virus disease indicates that in the immunocompromised patient there is an unusual presentation of a giant cell pneumonia with unusually large (up to 70 u) and occasionally multiple eosinophilic cytoplasmic inclusions. In this form of RS virus infection the amount and Buy Lithobid Online density of antigen present is comparable to that seen in the most extensive experimental infection of cell cultures. Staining of infected cell cultures with certain antisera demonstrated a hyaline cytoplasmic ring rich in RS virus antigen at the periphery of syncytial giant cells. This rim was resistant to dissolution even after extensive necrotic alteration of the remainder of the giant cell. This property of RS virus-induced giant cells makes possible the detection of residual ring-like structures within the endobronchial plugs of patients with fatal RS virus disease. These structures are visible in routine sections of lung tissue and are sufficient to suggest a diagnosis of RS virus disease. 23-62
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