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  4. what are the causes of Coxsackievirus infection and what are the causes of Coxsackievirus infection

what are the causes of Coxsackievirus infection and what are the causes of Coxsackievirus infection

what are the causes of Coxsackievirus infection and what are the causes of Coxsackievirus infection

The main cause of coxsackievirus infection: coxsackievirus

1. Pathogens

Coxsackie viruses can be divided into two categories according to their biological characteristics: Class A and Class B.. Echovirus and Poliomyelitis virus belong to enteroviruses. Now it is called "picoviruses".

2. Epidemiology

Dalldorf and Sickles (1948) first isolated the virus from Coxsachie, New York. Melnick (1949) Inoculating animals (mice) with this virus causes dyskinesia and limb paralysis. In humans, herpetic angina and non-paralytic poliomyelitis-like changes are caused.

3. Pathogenic mechanism

(1) The virus reproduces after entering the human body

Virus enters the host cell and decapitates, and directly replicates into polyprotein with molecular weight of 200kD. At the same time, protein synthesis of host cell is shut down. The mechanism of CV shutting down host protein synthesis is considered to be that viral protease 2A cleaves cell protein 17220 and inactivates starter complex Eit24F. La and other studies have found that CVB3 proliferates in a large number of myocardial cells, and the amount of infected virus is closely related to the degree of myocardial necrosis. CVB3, an early viral protein produced in infected cardiomyocytes, often blocks the synthesis of RNA and protein in myocardium. Accumulation of a large number of virus molecules in the late infection cycle, especially some capsid proteins such as VPl, directly leads to degeneration of myocardial cells, which changes the permeability of cell membrane and swells the cell body significantly. Finally, lysosomes of cells escape and autolytic cell digestion occurs.

(2) Virus affects myocardial metabolism

Virus infection of cardiomyocytes can directly lead to the loss of metabolizable energy of cardiomyocytes, and even cause cardiomyocyte death. Intracellular free CA 2 overload is one of the pathways leading to myocardial cell injury. Intracellular CA 2 overload inhibits cell systolic and diastolic function, activates intracellular calcium-dependent enzyme activity, promotes lipid peroxidation, and causes irreversible cell damage.

(3) The changes of adhesion molecules caused by virus infection

Adhesion molecules are a class of glycoproteins that exist on the surface of cells, and play a role in immune recognition, inflammatory reaction, cell adhesion and migration. The interaction between CVB3 and leukocytes plays an important role in the pathological process of viral myocarditis. CVB3 can infect mononuclear leukocytes and polymorphonuclear leukocytes, And produce infectious virus particles or polypeptides, CVB3 infection can up-regulate the expression of leukocyte functional antigen-1 (LFA-1) and its ligand intercellular adhesion molecule-1 (ICAM-1), and induce mononuclear cells to secrete mononuclear factors such as TNFa, IL-18 and IL-6, which can strongly promote the expression of adhesion molecules. The increase of adhesion molecules promotes the contact and adhesion between cells.

(4) Virus infection and apoptosis

Virus infection is an important factor regulating apoptosis. Zhao Guijun and others confirmed that virus infection can inhibit or promote apoptosis by expressing virus genes or activating apoptosis-related genes of host cells.

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