Nature: 'Semen can prevent Zika Virus Infection'
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The 2015-2016 Zika virus epidemic across the Americas became a huge healthcare scandal as it was one of the largest viral spreads this decade since swine flu (of South Asian origin) and Ebola (of West African origin). Originating somewhere in Brazil it was found that the method of transmission was caused mostly by mosquito vectors. Even though many victims can be asymptomatic mild to severe symptoms include rash, conjunctivitis, mild fever and even congenital microcephaly in newborns from infected pregnant mothers. An abundance of TNFa as part of the inflammatory pathway is responsible for some of these symptoms. Since this scare, even though rates have diminished there is no vaccine or cure yet for the disease - only recently a published trial using mice infected with the virus who suffer from seizures have had success using infliximab which is a TNFa inhibitor to reduce these seizures. Therefore investigations are underway to see if there are other routes of infection so we can prevent these occurrences from happening.
NatureCommunications published an article reporting recent experiments showing that whilst Zika virus (ZIKV) has broad cellular tropism, semen (which has high viral loads in ZIKV-infected individuals) inhibits ZIKV infection of cells and tissues from the anogenital region which surprisingly suggests that the spread of disease through sexual contact is not a route of transmission and is predominantly anthropod-mediated. Whilst other viruses spread by sexual contact, such as HIV-1 and CMV, because semen contains a positive charge on amyloid fibrils that concentrate the virions covered in a negatively charged membrane enhancing infection, ZIKV particles do not interact with the seminal amyloids. One proposed reason for this is that ZIKV particles are covered by a dense coat of viral E protein rendering the viral lipid membrane inaccessible to binding with other cells or factors - in contrast HIV-1 is only covered by a few glycoproteins. This proposition was shown by looking at results of infection rates using a cell-based immunodetection assay and fluorescence microscopy which altogether enzymatically quantifies flavivirus protein E levels. The specific factor which inhibits binding to the cellular target is yet to be determined but it is suggested that because similar experiments have shown that semen also inhibits DENV and WMV attachment there may be a similar novel attachment factor between them all. The experiments showed the anti-ZIKV inhibition in semen was independent of the donor efficiently inhibiting ZIKV GWUH and MR766. Also the paper suggests the factor inhibits an early step in the viral life cycle due to extracellular vesicle preparation. In turn all this leads to low-to-zero transmission of the virus into mucosal ports of entry which are the highly susceptible anogenital cells of the receiving partner.
The limitations of these postulations include that the results come from a small sample size and only study in vitro therefore animal studies are required to confirm the viral tropism inhibition effect and to determine the antiviral efficacy of the virus on anogenital infection in humans. Another alarming yet important investigation is knowing about whether ZIKV infection can acquire sperm resistance against the inhibitory factor(s) because this could lead to an increase in sexual-mediated transmission if factors render it to survive in conditions where arthropod-mediated transmission is rare.
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