Re: How hemaglutinin work
Coming from a slightly different tack I looked for other viruses that may be behaving in a similar with organ necrosis and sequestered host proteases.
Expression of factor X and its significance for the determination of paramyxovirus tropism in the chick embryo
The dancers are different but the dance is the same.
The virus is Paramyxovirus (Sendi or Newcastle), the protein being cleaved is F Glycoprotien and the protease is factor X (FXa another from the clotting cascade) and they used Russell?s Viper Venom another ?clot buster? to cleave FX into active FXa.
Viral graphic
and
Sendi Virus Symptoms (from http://ratguide.com/health/viruses/sendai_virus_sv.php)
Coming from a slightly different tack I looked for other viruses that may be behaving in a similar with organ necrosis and sequestered host proteases.
Expression of factor X and its significance for the determination of paramyxovirus tropism in the chick embryo
The dancers are different but the dance is the same.
The virus is Paramyxovirus (Sendi or Newcastle), the protein being cleaved is F Glycoprotien and the protease is factor X (FXa another from the clotting cascade) and they used Russell?s Viper Venom another ?clot buster? to cleave FX into active FXa.
Viral graphic
Enveloped animal viruses usually possess a surface glycoprotein which mediates fusion between the viral envelope and host cell membrane, hence enabling the
initiation of infection, and its biosynthesis often involves post-translational endoproteolytic activation of the inactive precursor by a host cell protease(s). Therefore, the protease distribution in the host must be critical for determining
the viral tropism. We previously isolated from chick embryo a cogent candidate endoprotease of this kind for paramyxovirus infection, and demonstrated its
identity with factor X (FX), a vitamin K-dependent serine protease in the prothrombin family which, in general, is synthesized in the liver and circulates as one of the
plasma proteases essential for blood clotting. Here, we examined FX expression with specific cDNA and antibody probes in a series of embryonic tissues. Many tissues
other than the liver expressed the specific mRNA but, in most instances, the translation products remained inactive zymogen forms. The enzymatically active FXa was detectable only in the allantoic fluid and amniotic fluid, and virus spreading was strictly confined to the tissues in direct contact with these FXa-containing fluids. Thus, the ectopically expressed FXa is probably the major host determinant of paramyxovirus tropism in ovo.
initiation of infection, and its biosynthesis often involves post-translational endoproteolytic activation of the inactive precursor by a host cell protease(s). Therefore, the protease distribution in the host must be critical for determining
the viral tropism. We previously isolated from chick embryo a cogent candidate endoprotease of this kind for paramyxovirus infection, and demonstrated its
identity with factor X (FX), a vitamin K-dependent serine protease in the prothrombin family which, in general, is synthesized in the liver and circulates as one of the
plasma proteases essential for blood clotting. Here, we examined FX expression with specific cDNA and antibody probes in a series of embryonic tissues. Many tissues
other than the liver expressed the specific mRNA but, in most instances, the translation products remained inactive zymogen forms. The enzymatically active FXa was detectable only in the allantoic fluid and amniotic fluid, and virus spreading was strictly confined to the tissues in direct contact with these FXa-containing fluids. Thus, the ectopically expressed FXa is probably the major host determinant of paramyxovirus tropism in ovo.
Identification of the responsible proteases would be difficult for the natural hosts, such as the mouse lung for Sendai virus and the human upper respiratory tract for
influenza A viruses. Earlier results suggested the importance of plasminogen activation by physiological and/or bacterial factors (Lazarowitz et al., 1973; Akaike et al., 1989). Furthermore, certain bacterial proteases could directly promote viral activation (Tashiro et al., 1987). FX of plasma origin could also be activated at the sites of tissue damage and inflammation. Moreover, activated macrophages were
shown to produce FXa (Osterud et al., 1980) or prothrombinase (Schwartz et al., 1982). The tryptase identified in mast cells has a substrate specificity very similar to that of FXa (Kido et al., 1985). Compared with plasmin and bacterial proteases, FXa obviously has a much more stringent substrate specificity and was found to cleave the viral precursors very efficiently (Gotoh et al., 1990). Thus, FXa and FXa-like proteases should also be taken into consideration as potential key enzymes for virus spread in natural hosts.
influenza A viruses. Earlier results suggested the importance of plasminogen activation by physiological and/or bacterial factors (Lazarowitz et al., 1973; Akaike et al., 1989). Furthermore, certain bacterial proteases could directly promote viral activation (Tashiro et al., 1987). FX of plasma origin could also be activated at the sites of tissue damage and inflammation. Moreover, activated macrophages were
shown to produce FXa (Osterud et al., 1980) or prothrombinase (Schwartz et al., 1982). The tryptase identified in mast cells has a substrate specificity very similar to that of FXa (Kido et al., 1985). Compared with plasmin and bacterial proteases, FXa obviously has a much more stringent substrate specificity and was found to cleave the viral precursors very efficiently (Gotoh et al., 1990). Thus, FXa and FXa-like proteases should also be taken into consideration as potential key enzymes for virus spread in natural hosts.
SV is a descending respiratory infection. It begins in the nasal passages, and moves through the trachea into the lungs. Sendai causes necrosis of the respiratory epithelium (thin layer of cells on the surface of the organs). In the first few days of infection epithelium necrosis is mild. As the disease progresses the necrosis becomes severe and usually peaks around day 5. By day 9 the regeneration of respiratory tract surface cells occurs. Focal interstitial pneumonia occurs and inflammation and lesions of varying degrees can develop on the lungs.
In uncomplicated infection the respiratory system shows evidence of healing within 3 weeks although there may be residual lesions, inflammation, or permanent scarring.
In uncomplicated infection the respiratory system shows evidence of healing within 3 weeks although there may be residual lesions, inflammation, or permanent scarring.
Originally posted by LMonty
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