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In a number of viruses with a viral envelope, viral receptors attach to the receptors on the surface of the cell and secondary receptors may be present to initiate the puncture of the membrane or fusion with the host cell. Following attachment, the viral envelope fuses with the host cell membrane, causing the virus to enter.
However, if a heart valve is damaged, the bacteria can attach themselves to the valve, resulting in infective endocarditis. Additionally, in individuals with weakened immune systems, the concentration of bacteria in the blood can reach levels high enough to increase the probability that some will attach to the valve.
It has been found to be important for the virus pathogenesis. [citation needed] In the case of Cardiovirus A, the virus can cause encephalitis and myocarditis, mostly in rodents, which are natural hosts. The virus is transmitted from rodents to other animals. Severe epidemics have been seen in swine and elephants. [9]
Infective endocarditis is an infection of the inner surface of the heart, usually the valves. [3] Symptoms may include fever, small areas of bleeding into the skin, heart murmur, feeling tired, and low red blood cells. [3] Complications may include valvular insufficiency, heart failure, stroke, and kidney failure. [4] [3]
Viruses enter host cells using a variety of mechanisms, including the endocytic and non-endocytic routes. [4] They can also fuse at the plasma membrane and can spread within the host via fusion or cell-cell fusion. [5] Viruses attach to proteins on the host cell surface known as cellular receptors or attachment factors to aid entry. [6]
The coronavirus can damage the heart, according to a major new study which found abnormalities in the heart function of more than half of patients.
[5] [6] [7] The protein encoded by this gene is a type I membrane receptor for group B coxsackie viruses and subgroup C adenoviruses. CAR protein is expressed in several tissues, including heart, brain, and, more generally, epithelial and endothelial cells.
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