The symptoms of many infectious diseases are caused by the intrusion of various pathogenic microorganisms into the animal body and the interaction with the host. However, when a microbe infects a host, the host certainly doesn't sit still. Usually the host has a set of defense mechanisms against invaders. For example, when a virus (invader) infects a cell (host), the protein kinase R (PKR) in the cell will be replaced by double-stranded RNA (double strand RNA, dsRNA). ) activates and further dephosphorylates the translation initiation factor eIF2α, so that translation is stopped, so that the virus cannot kidnap the cell's translation machinery to synthesize its own protein.
In this case, the virus has to find a way banner design to crack to save its life. For example, poxviruses exhibit two viral proteins to counteract the function of PKR: one is the viral E3L protein, which prevents the binding of dsRNA to PKR and prevents PKR from being activated; the other is the viral K3L protein, which Can prevent the phosphorylation of eIF2α by PKR. Scientists collectively refer to proteins such as E3L and K3L, which are used to counteract the host, as antagonists. According to the genetic material contained in the virus, viruses can be divided into two categories: DNA viruses and RNA viruses.
One of the biggest differences between the two viruses is that the mutation rate of RNA viruses is higher than that of DNA viruses. This is because the error rate when copying RNA is relatively high, but this increases the chance of new varieties (mutant varieties) of RNA viruses appearing, and virtually helps RNA viruses adapt to the environment (fitness). But poxvirus is a DNA virus, which is derived from cowpox virus that infects cattle, vaccinia virus that infects humans, and monkeypox virus that infects monkeys, all of which are zoonotic viruses. viruses). However, what scientists can't figure out is that poxviruses have to face such a diverse species, and there are different versions of PKR in each species, and poxviruses are DNA viruses with a low mutation rate, so when it invades the host , is how to cope with the host's resistance mechanism? Scientists at the Fred Hutchinson Cancer Research Center in Seattle knocked out the E3L gene of the vaccinia virus, and then used this E3L knockout virus to infect non-permissive cells of the pox virus— ─Human cervical cancer cells—These cells are not suitable for poxvirus replication. Two days later, the culture medium containing the new virus was collected, and the culture medium was used to infect new human cervical cancer cells. In this way, the infection cycle is repeated, and each infection is called a round or a passage.