Page 290 - Read Online
P. 290
Chen et al. Screening of genetic loci
background is polygenic, and HSV has no apparent Conflicts of interest
genetic background, the susceptibility of HSV infection There are no conflicts of interest.
itself is very likely regulated by more than one gene
controlling quantitative traits. Patient consent
There is no patient involved.
By bioinformatics analysis, our results suggest that
approximately 140 genes were found in the area of Ethics approval
D17MIT51.1, D17MIT39.1 and the genomic region Ethics approval was obtained prior to the
between D17MIT180.1 and D17MIT184, and functions commencement of the study.
of the majority of those genes are not fully revealed.
There is a possibility that the above sites are related REFERENCES
to the susceptibility to HSV infection, especially the
growth-related genes which are highly suggestive of 1. Lopez C. Genetics of natural resistance to herpesvirus infections in
the importance of genetic background. Among these mice. Nature 1975;258:152-3.
140 genes, there were about 33 genes homologous 2. Kirchner H, Kochen M, Munk K, Hirt HM, Mergenhagen SE,
to human genes. Their main functions include binding Rosenstreich DL. Differences in susceptibility to herpes simplex virus
infection of inbred strains of mice. IARC Sci Publ 1978;(24 Pt 2):783-8.
with other partners, regulating a variety of physiological 3. Lopez C. Resistance to herpes simplex virus - type 1 (HSV-1). Curr
processes, and the modulation of the phosphorylation Top Microbiol Immunol 1981;92:15-24.
process of various enzymes and coenzymes. 4. Cantin E, Tanamachi B, Openshaw H, Mann J, Clarke K. Gamma
interferon (IFN-gamma) receptor null-mutant mice are more
Based on our experimental results and bioinformatics susceptible to herpes simplex virus type 1 infection than IFN-gamma
analysis, the genetic background might play an ligand null-mutant mice. J Virol 1999;73:5196-200.
important role in susceptibility to HSV infection, which 5. Umene K, Yamanaka F, Oohashi S, Koga C, Kameyama T. Detection
is also consistent with most previous studies. It is worth of differences in genomic profiles between herpes simplex virus type 1
isolates sequentially separated from the saliva of the same individual.
noting that our finding is likely to be a quantitative J Clin Virol 2007;39:266-70.
trait locus, and may not be a particular system or 6. McLeod R, Buschman E, Arbuckle LD, Skamene E. Immunogenetics
population-specific mechanism. It is just a hint of this in the analysis of resistance to intracellular pathogens. Curr Opin
phenomenon in a particular system or population which Immunol 1995;7:539-52.
has a relative higher or lower incidence in another race 7. Smith MW, Dean M, Carrington M, Winkler C, Huttley GA, Lomb
or ethnic groups. This is not consistent with some DA, Goedert JJ, O’Brien TR, Jacobson LP, Kaslow R, Buchbinder
S, Vittinghoff E, Vlahov D, Hoots K, Hilgartner MW, O’Brien SJ.
previous research. Contrasting genetic influence of CCR2 and CCR5 variants on HIV-1
infection and disease progression. Hemophilia Growth and Development
In summary, the biological information and related Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter
data analysis suggest that these genes have important Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC),
physiological and pathological functions. However, ALIVE Study. Science 1997;277:959-65.
up to now, their associations with HSV susceptibility 8. Lagrange PH, Abel L. The genetic susceptibility to leprosy in humans.
infection have not been reported, suggesting that they Acta Leprol 1996;10:11-27. (in French)
could be potential candidate genes that contributed to 9. Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ,
Berman SM, Markowitz LE. Trends in herpes simplex virus type 1 and
the different susceptibility to HSV infection. type 2 seroprevalence in the United States. JAMA 2006;296:964-73.
10. Fatahzadeh M, Schwartz RA. Human herpes simplex virus infections:
Because HSV infection phenotypes have not been epidemiology, pathogenesis, symptomatology, diagnosis, and
clearly defined yet, some issues are far from a management. J Am Acad Dermatol 2007;57:737-63; quiz 764-6.
consensus. For instance, whether the differences in 11. Garland SM, Steben M. Genital herpes. Best Pract Res Clin Obstet
response to HSV infection really exist and whether the Gynaecol 2014;28:1098-110.
genetic background plays a role in it. All these issues 12. Thompson RL, Sawtell NM. The herpes simplex virus type 1 latency-
will undoubtedly limit the objectivity of this research. associated transcript gene regulates the establishment of latency. J
Virol 1997;71:5432-40.
It is also necessary to validate the results in the 13. Nash AA, Cambouropoulos P. The immune response to herpes
present study by expanding the sample size, further simplex virus. Semin Virol 1993;4:181-6.
investigating the role of the regulatory regions in 14. Rouse BT, Babiuk LA. Mechanisms of recovery from Herpesvirus
regulating susceptibility to HSV infection. Furthermore, infections - a review. Can J Comp Med 1978;42:414-27.
the functions of genes near these microsatellite loci, 15. Posavad CM, Koelle DM, Shaughnessy MF, Corey L. Severe genital
as well as their functions in regulating susceptibility, herpes infections in HIV-infected individuals with impaired herpes
simplex virus-specific CD8+ cytotoxic T lymphocyte responses. Proc
deserve further investigation. Natl Acad Sci U S A 1997;94:10289-94.
16. Biron CA. Initial and innate responses to viral infections -- pattern
Financial support and sponsorship setting in immunity or disease. Curr Opin Microbiol 1999;2:374-81.
Nil. 17. Pien GC, Nguyen KB, Malmgaard L, Satoskar AR, Biron CA. A
Neuroimmunology and Neuroinflammation ¦ Volume 3 ¦ December 26, 2016 281