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Viral pathogenesis is affected by various factors: (1) transmission, entry and spread within the host, (2) tropism, (3) virus virulence and disease mechanisms, (4) host factors and host defense. [ 4 ]
For example, viroplasms of mimivirus have a similar size to the nucleus of its host, the amoeba Acanthamoeba polyphaga. [9] A virus can induce changes in composition and organization of host cell cytoskeletal and membrane compartments, depending on the step of the viral replication cycle. [1]
DNA templated transcription, with some alternative splicing mechanism is the method of transcription. The virus may exit the host cell by vesicular trafficking following nuclear pore export or be released following cell lysis. Mustelids, skunk, and raccoons serve as the natural host. [11] [10] Transmission routes are oral and respiratory. [6]
In Denmark, there have been five clusters of mink variants of SARS-CoV-2; the Danish State Serum Institute (SSI) has designated these as clusters 1–5 (Danish: cluster 1–5). In Cluster 5, also referred to as ΔFVI‑spike by the SSI, [8] several different mutations in the spike protein of the virus have been confirmed.
A lethal infection in mink, the Aleutian disease virus lies dormant in ferrets until stress or injury allows it to surface. While the parvovirus itself causes little or no harm to the ferret host, the large number of antibodies produced in response to the presence of the virus results in a systemic vasculitis, resulting in eventual renal failure, bone marrow suppression and death. [10]
An infectious disease agent can be transmitted in two ways: as horizontal disease agent transmission from one individual to another in the same generation (peers in the same age group) [3] by either direct contact (licking, touching, biting), or indirect contact through air – cough or sneeze (vectors or fomites that allow the transmission of the agent causing the disease without physical ...
To enter the cells, proteins on the surface of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or its genetic contents are released into the host cell, where replication of the viral genome may commence.
The virus replicates in the cells of the crypt epithelium in the duodenum and jejunum and, to a lesser extent the ileum, colon and caecum. The severity of the disease is directly related to necrosis of the crypt epithelium. [2] Virus enteritis of mink was recognized first in 1947 when epizootics occurred among ranch mink in southern Canada.