Page 289 - Read Online

Chen et al. Screening of genetic loci

Figure 2: The microsatellite loci scan results of two DBA-2 mouse lines. A: D17MIT245.1; B: D17MIT143.2; C: D17MIT46; D: D17MIT46.1; E:
D17MIT51.1; F: D17MIT10.1; G: D17MIT180.1; H: D17MIT20.1; I: D17MIT18; J: D17MIT93; K: D17MIT39.1; L: D17MIT122.1
As a viral disease seriously affecting human health to closely correlate with the complex viral genome
with an increasing incidence in recent years, herpes structures and the molecular mechanism of viral gene
simplex virus 1 (HSV-1) infection typically generates transcriptional regulation and replication. [19,20]
uncomfortable, watery blisters on the skin or mucous
[1]
membranes of the mouth and lips, [9,10] potentially leads In fact, as early as 1975, Lopez reported that there
to encephalitis with remarkable sequelae, or vesicle are significant differences in the genetic backgrounds
[11]
eruption on genital organs. More importantly, the of inbred mice that had significantly different
eruption of these blisters and vesicles are frequently reactions to the same or similar HSV infection, which
attributed to the long-term latent infection of HSV-1 undoubtedly suggested that genetic background
in the nervous system. Although the human HSV might be an important factor for susceptibility to
[12]
infection rate is very high, it is difficult to fully attract infection. This mechanism revealed by Lopez has
people’s attention, so it’s difficult for us to associate also been confirmed by other studies. [2,3] Also, there
HSV infection with genetic background. Therefore, was a follow-up study on the relationship between
most of the previous HSV infection studies focused the genetic background and susceptibility to HSV
on the acquired immune response after infection, infection. Zawatzky et al. showed that compared
[21]
showing that T cell-mediated immune response plays with susceptible DBA/2 mice, the relatively tolerant
an important role in resisting HSV-1 infection, [13,14] and C57BL/6 mice could produce more interferons in the
immune suppressed or immune deficient individuals immune response when it comes to HSV-1 infection.
are vulnerable to opportunistic herpes virus infection. But Brenner et al. showed that there is no significant
[15]
[22]
Furthermore, recent studies [16,17] suggested that innate difference in the immune response to HSV infection
immune response plays a key role in limiting the spread among those two mouse lines. If the findings in
[23]
of the virus. The development of innate immune germ mortality after infection phenotype, Simmons et al.
line occurs earlier than acquired immune response reported that only one gene loci functions in this
system, and these two mechanisms function process, while Kastrukoff et al. reported that there
[24]
[18]
differently. This is undoubtedly an important point that were two loci separated in the role. We are inclined to
genetic backgrounds play an important role in HSV believe that from the viewpoint of a gene associated
infection. Meanwhile, the clinical symptoms of acute with genetic background, it is undoubtedly that genetic
infection, as well as the long-term pathologic processes background plays an important role in the phenotypic
induced by recurrent latent infection, have been shown susceptibility to HSV infection. Since the genetic
280 Neuroimmunology and Neuroinflammation ¦ Volume 3 ¦ December 26, 2016