Zika virus outbreak could spread rapidly due to one mutation study

Wednesday, April 13, 2022
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Zika Virus Outbreak Could Be Accelerated Due to One Mutation Study

A new study suggests that the Zika virus can be genetically modified to the point that previous dengue infection is no longer effective. This mutation is theoretical‚ but further research is needed to find out whether the virus is dangerous to humans. The study explains that one mutation in the Zika virus was able to change a mouse's immune system to the point that it is no longer effective. The virus' transmission probability could increase exponentially if this mutation is found in the wild.

Molecular cloning

One mutation in the genome of the Zika virus has made the infectious clone of the virus extremely stable. But one mutation in a different gene is enough to cause it to spread rapidly. Using this mutation‚ scientists have been able to develop an infected cell line that is highly infectious to Aegypti mosquitoes. The results of this study suggest that the virus is a highly effective vector for spreading the virus. For the pEGFP-N1 vector‚ a cytomegalovirus promoter sequence was amplified using the same bacterial primer. This promoter sequence was fused to the genomic sequence of Zika virus‚ which is 1-5908 nt long. The PCR product was then screened using a chloramphenicol-based LB agar plate. Previously‚ ZIKV infection was limited to Africa and Asia. In many cases‚ infection was asymptomatic‚ with just a few affected patients exhibiting maculopapular rash and mild joint pain. Now‚ there are growing concerns about the spread of the virus‚ and there are multiple routes of infection. The study suggests that ZIKV's evolution has changed over time to adapt to its new environments. Using a mouse model‚ researchers found that the E-V473M mutation increased the fitness of Aedes aegypti mosquitoes‚ even though it did not affect their oral infection. The V473M mutation is located in the second transmembrane helix of the E protein. It enhances virion morphogenesis. In addition to improving the virulence of ZIKV‚ it has also been shown to be important for intrauterine transmission during pregnancy. The study also suggests that a similar mutation would facilitate urban transmission of the virus. The results of this study indicate that the Asian and African lineages share similar brain-development disruption. However‚ it remains to be seen whether these mutations have a common impact on the spread of Zika virus. Further research needs to be done to discover whether one mutation is enough to change its spread. The study also recommends that ZIKV be studied using more Asian and African strains.

Genetic mutation

The new research shows that the Zika virus outbreak could be accelerated by genetic mutations in the virus's genome. The study used publicly available genomic data and in-vivo laboratory studies to examine the spread of the disease. Researchers found that these changes increased the disease's capacity for urban transmission. These changes are an important factor in determining where outbreaks are likely to emerge. Further research is needed to understand the implications of these findings for future outbreaks. Scientists from the La Jolla Institute for Immunology have discovered a new genetic mutation in the Zika virus. This mutation is highly infectious and can break through any preexisting immunity in people. The virus is spread by mosquitoes and causes mild symptoms in adults. However‚ it can cause birth defects if it infects an unborn baby. This new research shows that the disease could be spread quickly if the virus can reach the fetus. The researchers used DNA sequencing technology to examine the genetic differences between the current human and mosquito strains of Zika. They compared the nucleotide sequences of 41 different Zika virus strains. Twenty-one of these strains were derived from humans while ten came from mosquitoes. Genetic studies showed that both the Asian human strain and the African mosquito strains had a panel of mutations. The researchers believe that these changes are responsible for the recent outbreaks in Asia and the South Pacific. While ZIKV has shown significant fitness loss when introduced to Asia‚ its fitness has been partially restored after introduction into the Americas. The resulting microcephaly is caused by a mutation in the NS1 pre-membrane protein. These mutations also increase the virus's virulence in non-human primates. Interestingly‚ this study suggests that the changes could lead to an even larger Zika virus outbreak. Genetic mutations play a major role in the spread of an outbreak of ZIKV. This study also found that an NPC with the genotype of four revertant mutations was associated with an increase in the risk of the virus spreading to other areas. This study is important because it will allow researchers to investigate the role of host genetics in spreading the Zika virus epidemic. If the findings prove to be correct‚ more studies in Asia could be conducted.

Transmission probability

A mutation in the E protein of the Zika virus may have a strong influence on its rapid spread. The study shows that a mutation in E may have altered the susceptibility of mosquitoes to the arbovirus. The mutation is at the second transmembrane helix and enhances virion morphogenesis. Although it has been known that the virus is primarily transmitted through mosquitoes‚ it may also be transferred from mother to child or through saliva. The transmission probability of a Zika virus outbreak may have increased due to a single mutation in the Asian strain. However‚ it is difficult to estimate the size of a ZIKV outbreak because most cases are asymptomatic. Nevertheless‚ the rapid spread of the disease in North America and the large distance it has travelled since its discovery suggests that the virus might be a novel STD. The findings have implications for global health. A Zika virus outbreak that was detected in 2015 may be an example of an unforeseen‚ sudden epidemic. The reduction of symptomatic cases in recent years suggests that the virus is in remission or is no longer a threat. However‚ the Stockholm Paradigm outlines a cycle of expansion‚ evolution‚ and change in transmission and virulence. This evolutionary scenario assumes that the asymptomatic strains are sexually transmitted. The findings suggest that nonhuman primates in South America may be susceptible to the Zika virus. This study found that the aedes mosquito carries a mutation in the envelope protein that increases the viral neurovirulence‚ maternal-to-fetal transmission‚ and viremia. However‚ it has yet to be proved that these mutations in nonhuman primates could be the cause of an outbreak. The UCLA researchers also observed that a particular mutation in the NS1 protein disrupts the central hydrogen bonding network. In vitro‚ this mutation may destabilize NS1 dimeric assembly. Further studies are needed to determine the relevance of this mutation for human health. This finding is significant for the global health community. The Zika virus is already associated with microcephaly‚ but its symptoms are few.

Infectious clones

The latest research suggests that a single mutation in ZIKV‚ S139N‚ may play a major role in the virulentity of this mosquito-borne disease. The researchers say this mutation significantly enhances the virus's infectivity in human NPCs and causes a greater risk of microcephaly in fetal mice. The results suggest that this mutation first emerged in Southeast Asia in May 2013‚ and has since stably been maintained in the epidemic strain throughout its spread to the Americas. The research was supported by the National Institutes of Health‚ the Sealy & Smith Foundation‚ and the John S. Dunn Foundation. Prof. Jonathan Ball‚ who specializes in viruses‚ says that the mutation study could lead to the identification of new coronavirus variants. By understanding this mutational pattern‚ scientists could intervene early to prevent the outbreak from spreading. Meanwhile‚ a recent study by LLNL biologist Nicole Collette suggests that a previous infection to the virus may still provide protection against the new variants. The study found that the mutation in the virus occurred in mouse cells exposed to dengue and those that had not. This mutation is located in the same part of the virus's genome as the dengue virus. The researchers also found that the mutation was more virulent and infectious than the original virus. The mutation in Zika virus could also help the mosquito virus escape the dengue protective coating that the dengue virus enjoys. The findings of this study suggest that the genetics of the virus are related to the geographic origins of the disease. Asian strains of Zika are more likely to be transmitted to people by mosquitoes‚ whereas African strains are less likely to spread by air. This means that the disease could spread to other countries if a virus was introduced to one region and then introduced to another. This is an extremely concerning development‚ but it is worth noting. In a lab study‚ scientists discovered that a specific ZIKV variant had undergone a genetic change that made it a more aggressive virus. The mutation was so small that the mice with the dengue-infection did not develop cross-protective immunity against it. This suggests that Zika could re-emerge in places where dengue fever is already widespread. And this means an outbreak could be even more severe in the US.