how does the virus cause the disease?



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A team of scientists studied what happens in monkeys when they are infected with SARS-CoV-2 and how the monkey can make us sick.

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To properly diagnose and treat an infectious disease, it is necessary to know the behavior of the affected infectious agent within our body and the damage it causes. Since the beginning of pandemic, several monkey studies have been conducted to answer the questions posed on this topic. The results obtained are not consistent. In some experiments we find lung lesions, in others edema it’s a inflammation alveolar. Usually, as in humans, the infection shows no serious clinical signs. In a recent study published in The Journal of Infectious Disease, the researchers developed an experimental method and a promising animal model for studying interactions between SARS-CoV-2 and the immune system.

A rigorous experience

The researchers needed sixteen monkeys for their experiment, male and female. They took care to choose several Cash with variability genetics and immunological between them to mimic the variability that can exist between us humans. Moreover, even scientists have done it vary the dose of the infectious inoculum and the mucous membranes through which SARS-CoV-2 entered the body (trachea, mouth, eyes, nostrils, intravenous). Finally, the virus inoculated was from a Korean patient infected with SARS-CoV-2.

Subsequently, the experimenters undertook several measures: blood tests, clinical signs, behavioral analysis through locomotor measurements and tissue and immune response analyzes. Most of the animals were slaughtered, tired and feverish like most of the infected humans by SARS-CoV-2. Few changes were noted in terms of weight and frequency respiratory. Not surprisingly, the preferred site for the virus to replicate was the airways.

During post mortem examinations, they observed lung damage associated with signs of pneumonia interstitial similar to previous data in humans and monkeys. In all animals, the researchers also found transient endothelitis and lymphopenia. Due to the similarity between the human immune system and that of signs, the authors suggest that their experimental model may also be suitable for studying interactions between SARS-CoV-2 and the immune system. They suggest that it could be used to validate the effect of immunomodulators in conjunction with therapeutic approaches to improve observed lymphopenia.

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