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Table of Contents   
LETTER TO THE EDITOR  
Year : 2017  |  Volume : 10  |  Issue : 2  |  Page : 458-459
Zika virus infection: Factor contributing to emergence and pathogenesis


1 Wiwanitkit House, Bangkhae, Bangkok, Thailand
2 Hainan Medical University, Haikou, Hainan, China

Click here for correspondence address and email

Date of Web Publication22-Jun-2017
 

How to cite this article:
Wiwanitkit S, Wiwanitkit V. Zika virus infection: Factor contributing to emergence and pathogenesis. Ann Trop Med Public Health 2017;10:458-9

How to cite this URL:
Wiwanitkit S, Wiwanitkit V. Zika virus infection: Factor contributing to emergence and pathogenesis. Ann Trop Med Public Health [serial online] 2017 [cited 2019 Nov 14];10:458-9. Available from: http://www.atmph.org/text.asp?2017/10/2/458/208734
Dear Sir,

The situation of Zika virus infection is very interesting. Barzon et al. noted that “factors involved in virus emergence are still unknown, but probably included the introduction in naïve environments characterized by the presence of high densities of competent Aedes spp. mosquitoes and susceptible human hosts in urban areas.''[1] Barzon et al. also noted that “diagnosis relies on the detection of viral nucleic acids in biological samples, while detection of a specific antibody response may be inconclusive because of the broad cross-reactivity of antibodies among flavi viruses.”[1] Indeed, the emergence of Zika virus infection might be caused by several factors. The presence of high densities of competent Aedes spp. mosquitoes might be an important factor. However, in some setting, there is no high density of vectors but the problem occurs. The good example is the recent emergence of disease in Singapore.[2]

On the other hand, in some areas with high densities of vectors (such as Thailand), there is still no outbreak of Zika virus infection. In addition, the Zika virus can also be transmitted by other non-vector modes of transmission including sexual contact and blood transfusion. Further local transmission of disease in the setting where there is no mosquito can be expected. The role of non-vector mode of transmission should not be forgotten. Focusing on the susceptible of host in urban area to arboviral disease, it might not correct that the people in urban areas are more susceptible to the infection. For dengue, a highly similar arboviral infection to Zika virus infection, the infection rate per population density in urban and rural area is not different. The important factor that might contribute to the difference in infection rate should be the environmental factor. For example, rainfall [3] and humidity [4] are proved to be important determinant for Zika virus infection rate. The genetic factor might also have the effect on the susceptibility to Zika virus infection. In fact, this topic that is largely unknown. It is still the unexplained question on the epidemiological difference of the infection between South America and other areas of the world, especially for tropical Asia. There is a big difference in incidence of symptomatic infection, congenital microcephaly, and neurological complication.[5],[6] A possible difference might be explained by the difference of viral strain. In a recent publication by Zhang et al. on Asian ZIKV C and African ZIKV M, the difference due to different strains is reported.[7] Zhang et al. observed that “while overall expression profiles are similar, ZIKV C, but not ZIKV M, induces upregulation of viral response genes and TP53” and “P53 inhibitors can block the apoptosis induced by both ZIKV C and ZIKV M in hNPCs, with higher potency against ZIKV C-induced apoptosis.''[8] Focusing on the pathogenesis of Zika virus infection, the animal models show the evidence that “the virus can infect and efficiently replicate in the placenta and in the brain and induced foetal demise or neural damage.''[1] In fact, the direct neurological pathology caused by virus invasive can be explained by the nanostructure of virus and placenta.[8]

Some researchers also mentioned the role of the immunopathogenesis. A recent report [9] mentioned that the “dengue virus sero-cross-reactivity drives antibody dependent enhancement of infection with Zika virus.” This theory can be supported by the similarity between structure of Zika virus and dengue. This theory might explain the high rate of missed diagnosis of Zika virus infection as dengue infection [10] and confirmed the need for molecular diagnosis of Zika virus.[1] However, in the area with high dengue prevalence and confirmed cross-immunoreactivity between Zika virus and dengue infection, such as Thailand there is still no problem of Zika virus outbreak.[11] As a conclusion, any presently available propose pathological processes are not valid for explanation of the epidemiological difference of Zika virus infections in different regions of the world. Whether there is any genetic or environmental factor in South America that contribute to the clinical problems is the interesting question for further study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Barzon L, Trevisan M, Sinigaglia A, Lavezzo E, Palú G. Zika virus: From pathogenesis to disease control. FEMS Microbiol Lett 2016;pii: fnw202. [Epub ahead of print]  Back to cited text no. 1
    
2.
Dyer O. Outbreak of Zika in Singapore sparks warnings in neighbouring countries. BMJ 2016;354:i4740.  Back to cited text no. 2
    
3.
Wiwanitkit S, Wiwanitkit V. Predicted pattern of Zika virus infection distribution with reference to rainfall in Thailand. Asian Pac J Trop Med 2016;9:719-20.  Back to cited text no. 3
    
4.
Joob B, Wiwanitkit V. Humidity that is appropriate for Zika virus infection: A summary from Thai cases. Asian Pac J Trop Med 2016;9:721.  Back to cited text no. 4
[PUBMED]    
5.
Sriwijitalai W, Wiwanitkit V. Zika virus infection in pregnant women: topic for discussion. Rev Bras Ginecol Obstet 2016;38:314.  Back to cited text no. 5
[PUBMED]    
6.
Wiwanitkit V. Guillain-Barré syndrome and Zika virus infection. Arq Neuropsiquiatr 2016a;74:692.  Back to cited text no. 6
    
7.
Wiwanitkit V. Placenta, Zika virus infection and fetal brain abnormality. Am J Reprod Immunol 2016b;76:97-8.  Back to cited text no. 7
    
8.
Zhang F, Hammack C, Ogden SC, Cheng Y, Lee EM, Wen Z, et al. Molecular signatures associated with ZIKV exposure in human cortical neural progenitors. Nucleic Acids Res 2016; pii: gkw765. [Epub ahead of print].2016;44:8610-8620.  Back to cited text no. 8
    
9.
Dejnirattisai W, Supasa P, Wongwiwat W, Rouvinski A, Barba-Spaeth G, Duangchinda,et al. Dengue virus sero-cross-reactivity drives antibody-dependent enhancement of infection with zika virus. Nat Immunol 2016;17:1102-8.  Back to cited text no. 9
    
10.
Joob B, Wiwanitkit V. Zika virus infection and dengue: A new problem in diagnosis in a dengue-endemic area. Ann Trop Med Public Health 2015;8:145-6.  Back to cited text no. 10
  [Full text]  
11.
Wikan N, Suputtamongkol Y, Yoksan S, Smith DR, Auewarakul P. Immunological evidence of Zika virus transmission in Thailand. Asian Pac J Trop Med 2016;9:141-4.  Back to cited text no. 11
    

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Correspondence Address:
Somsri Wiwanitkit
Wiwanitkit House, Bangkhae, Bangkok
Thailand
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.208734

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