Principles of Virology, Volume 2. S. Jane Flint

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Principles of Virology, Volume 2 - S. Jane Flint


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2.13).

      Researchers have found that Zika virus genetic material can be identified in tears of infected mice. This finding perhaps explains why some Zika-infected patients develop uveitis, a serious eye disease that can lead to permanent blindness, as well as less serious eye disorders such as retinal damage or optic nerve inflammation. Moreover, detection of viral nucleic acid in tears suggests that the eye might be a reservoir for Zika, and thus a portal for virus shedding. Of note, this has yet to be confirmed in humans, and presence of genetic material does not indicate that infectious virus is present. Nevertheless, the identification of a new potential “way out” for viruses indicates that viruses may be able cross numerous host barriers to access tear ducts, and may pose challenges for commonplace procedures such as corneal transplants. Adenoviruses can also be found in tears of individuals suffering from “pink eye,” the common name given for adenoviral conjunctivitis.

      Despite the complexity and diversity of viral infection cycles, at a minimum, all viruses must get in, and they must get out. This is true not only for infections of the cell (a major theme of Volume I) but also for infections of the host. In this Chapter, we discussed the many ways by which an organism may acquire pathogens. It is not hyperbole to note that pathogens, including viruses, bacteria, eukaryotic parasites, and fungi, are truly everywhere, and because they have coevolved with their hosts, all have coopted our behaviors to ensure host-to-host transmission.

      Fortunately, our counter-defenses pose formidable obstacles. Viruses are trapped in mucus, repelled by dead layers of skin, brushed away by cilia, and destroyed by stomach acid. However, capturing a rook and a bishop does not end this age-old game of chess. Some viruses can bypass these defenses to reach target cells deep within organs. When viruses breach our formidable barriers, it is up to the elite forces of the host immune system, the precise strategies of the intrinsic, innate, and adaptive responses, to either end the game in checkmate or suffer the fateful capture of the king.

      DISCUSSION

       Chicken pox parties

      Prior to the widespread use of the varicellazoster virus vaccine, some parents who wanted to control when their child would get chicken pox (mistakenly considered a childhood “rite of passage”) would host chicken pox parties, in which uninfected children would share lollipops licked by infected children. Given the presence of the virus in the oral mucosa, this practice ensured that the lollipop contained a high dose of the virus and virtually guaranteed infection. Moreover, because the incubation period for varicella is quite precise (about 14 days following exposure), parents could preplan days of from work to be with their sick child. Even today, there is a “black market” of virus-laced items (such as lollipops) available through the Web. Such practices are an almost inconceivably bad idea; infections by these viruses can be quite severe, and effective, safe vaccines do exist. Moreover, infected children pose risks to immunocompromised individuals, such as the elderly and cancer patients receiving immunosuppressive chemotherapy.

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       Books

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       Review Articles

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      Cadwell K. 2015. The virome in host health and disease. Immunity 42:805–813.

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      Coyne CB, Lazear HM. 2016. Zika virus—reigniting the TORCH. Nat Rev Microbiol 14:707–715.

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      Esteban DJ, Buller RM. 2005. Ectromelia virus: the causative agent of mousepox. J Gen Virol 86:2645–2659.

      Keele BF, Estes JD. 2011. Barriers to mucosal transmission of immunodeficiency viruses. Blood 118:839–846.

      Kennedy PGE. 1992. Molecular studies of viral pathogenesis in the central nervous system: the Linacre Lecture 1991. J R Coll Physicians Lond 26:204–214.

      Ku CC, Besser J, Abendroth A, Grose C, Arvin AM. 2005. Varicella-zoster virus pathogenesis and immunobiology: new concepts emerging from investigations with the SCIDhu mouse model. J Virol 79:2651–2658.

      Lancaster KZ, Pfeiffer JK. 2012. Viral population dynamics and virulence thresholds. Curr Opin Microbiol 15:525–530.

      Malamud D, Abrams WR, Barber CA, Weissman D, Rehtanz M, Golub E. 2011. Antiviral activities in human saliva. Adv Dent Res 23:34–37.

      Pereira L, Maidji E, McDonagh S, Tabata T. 2005. Insights into viral transmission at the uterine-placental interface. Trends Microbiol 13:164–174.

      Samuel MA, Diamond MS. 2006. Pathogenesis of West Nile virus infection: a balance between virulence, innate and adaptive immunity, and viral evasion. J Virol 80:9349–9360.

      Tellinghuisen TL, Evans MJ, von Hahn T, You S, Rice CM. 2007. Studying hepatitis C virus: making the best of a bad virus. J Virol 81:8853–8867.

      Virgin HW. 2007. In vivo veritas: pathogenesis of infection as it actually happens. Nat Immunol 8:1143–1147.

      Wiens ME, Wilson SS, Lucero CM, Smith JG. 2014. Defensins and viral infection: dispelling common misconceptions. PLoS Pathog 10:e1004186.


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