Virology Club


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فک میکنم اینطوریه ک لفظ طاعون بطورکلی واسه بیماریهایی بکار میره ک پاندمی میده و جون افراد زیادی رو میگیره، درسته ک مشخصا ما برای بیماری ای ک یرسینیا میده بکار میبریم ولی مثلا انفلوانزای 1918 رو هم طاعون میگن چون حدود 50 میلیون نفر جونشونو از دس دادن

یکی از معانی لغت pest نیز از همینجا میاد ... >>> [/COLOR]* طاعون *

vet lab sciences

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Model of filovirus pathogenesis in primates.jpg

Model of filovirus pathogenesis in primates
Monocytes, tissue macrophages, and dendritic cells appear to be early and preferred sites of filovirus replication. Soluble factors released from virus-i nfected mononuclear cells act locally and systemically. Release of chemokines from these virus-infected cells recruits additional monocytes and macrophages to sites of infection, making more target cells available for viral exploitation and further amplifying an already dysregulated host response. In addition, these soluble factors contribute to the impairment of the vascular system. Although filoviruses do not productively infect lymphocytes, the rapid loss of lymphocytes by the process of apoptosis is a noted feature of disease. This lymphocyte loss is probably due to a combination of factors including virus-induced impairment of dendritic cell function, release of proapoptotic soluble factors from virus-infected monocytes and macrophages, and possibly direct interaction between viral antigens and lymphocytes. Coagulation abnormalities are consistent features of filovirus disease and are caused by a number of factors, particularly during the later stages of disease; recent data strongly implicate a role for tissue factor. The hemodynamic and coagulation disorders are exacerbated by infection of hepatocytes and adrenal cortical cells, resulting in impairment in the synthesis of important clotting factors. At the same time, impaired secretion of steroid-synthesizing enzymes by virus-infected adrenal cortical cel ls leads to hypotension. DC, dendritic cell; NO, nitric oxide. (Adapted from a prior publication by Bray M, Geisbert TW. Ebola virus: the role of macrophages and dendritic cells in the pathogenesis of Ebola hemorrhagic fever. Int J Biochem Cell Biol 2005;37:1 560-1 566

vet lab sciences

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Pathologic features seen in the liver of an EBOV-infected

A: Sinusoidal dilation and congestion and hepatocellular necrosis (H&E, 250X).Numerous filamentous intracellular ZEBOV inclusion (arrows) are seen in association with an area of coalescent hepatic necrosis. B: Heavy immunohistochemical staining of ZEBOV antigens are seen in sinusoids, sinusoidal lining cells, and hepatocytes (arrows) (immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain, 1 58x). C: Electron micrograph of liver showing several large EBOV inclusions within infected hepatocytes (uranyl acetate and lead citrate stain, 6,600x). Abundant extracellular EBOV particles are also seen in hepatic sinusoids. Note variation in size and shape of viral
particles associated with necrotic debris