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Editorial

A brief review on the immunological responses to zika virus infection in humans

Subha Ganguly1*, Rajesh Wakchaure2

1Department of Veterinary Microbiology, 2Department of Animal Genetics & Breeding, Arawali Veterinary College, N.H. – 52 Jaipur Road, V.P.O. Bajor, Sikar – 332001, Rajasthan, India

*For correspondence

Dr. Subha Ganguly,

Associate Professor, Department of Veterinary Microbiology, Arawali Veterinary College, N.H. – 52 Jaipur Road, V.P.O. Bajor, Sikar – 332001, Rajasthan, India.

Email: ganguly38@gmail.com

Received: 28 August 2016

Accepted: 22 September 2016

ABSTRACT

Zika virus is categorized under the virus family Flaviviridae and the genus Flavivirus. The virus is transmitted via Aedes mosquitoes, such as A. aegypti which remain active during daytime. The name of the etiology is derived from the Zika Forest of Uganda from where the virus was first isolated in 1947. The extrinsic incubation period of the virus in the vector is about 10 days. The virus is transmitted by the mosquitoes belonging to the genus Aedes.

 

 

 

Keywords: Immunology, Mosquito-borne, Transcription, Zika virus

Introduction

Zika virus generally infects the skin dendritic cells in particular.1,2 Hamel et al.2 explored by exposing Zika virus to human skin cells to know the immunolgical reactions after exposure to an infected mosquito. It was revealed that Zika appears to use the C-type lectin receptor, DC-SIGN and members of the TIM and TAM families of phosphatidylserine receptors on host cell surface to gain access to the cytoplasm via receptor-mediated endocytosis. This indicates that immature dendritic cells, dermal fibroblast and keratinocytes can be infected and support this viral replication.

Immune response generated in the virus infection

An innate immune response is triggered by the virus in infected primary human fibroblasts. Type 1 and type 2 interferons trigger the inhibition of zika viral replication. At the molecular level TLR3 recognizes the double-stranded RNA. Initial investigations suggested that at the cellular level the virus induces autophagosome formation to promote replication and may trigger apoptosis to foster viral dissemination.2-4

Serosurvey report in Thailand

Wikan et al.4 carried out a preliminary serosurvey of possible exposure to Zika virus was with 21 serum samples of patients suffering from fever. These were examined for immunoreactivity to Zika virus envelope antigens by Western blot analysis. The results revealed that only two sera samples showed immunoreactivity only to Zika envelope antigen. The first evidence of Zika virus transmission was present through this study in Thailand. Further investigation is demanded in the interrelationship between zika virus transmission and possible cases of Zika fever in Thailand.4

Transcription of the virus

The transcription of Toll-like receptor 3 (TLR3), MDA5 and RIG-I, including several interferon-stimulated genes, viz., OAS2, MX1 and ISG15 has resulted due to zika virus infection. It is characterized by the expression of beta interferon gene. Autophagosomes are formed due to skin fibroblast infection and increased viral replication. Several entry and/or adhesion factors, including AXL, Tyro3, DC-SIGN and TIM-1 to a lesser extent are helpful in allowing entry of zika virus with a major role for the TAM receptor AXL.2,5,6.

Conclusions

The virus can be transmitted from a healthy to suspected human being by sexual contacts and across the placenta to the foetus. It is believed that the virus have a relation with microcephaly in newborn babies which is vertically transmitted from infected mother to newborn/ child.

Funding: No funding sources

Conflict of interest: None declared

References

  1. Ganguly S, Wakchaure R, Para PA, Praveen PK, Sahoo S. An overview on the latest pandemic outbreak of Zika virus in 2016 and its implications to human health. Int J Pharm Biomed Res. 2016;3(1):7-8.
  2. Hamel R, Dejarnac O, Wichit S, Ekchariyawat P, Neyret A, Natthanej, et al. Biology of zika virus infection in human skin cells. J Virol. 2015;89(17):8880-96.
  3. Hoffmann AA, Montgomery BL, Popovici J, Iturbe-Ormaetxe I, Johnson PH, Muzzi F, et al. Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission. Nature. 2011;476:454–7.
  4. Wikan N, Suputtamongkol Y, Yoksan S, Smith DR. Immunological evidence of Zika virus transmission in Thailand Asian Pacific Journal of Tropical Medicine. 2016;9(2):141–4.
  5. Jin J, Liss NM, Chen DH, Liao M, Fox JM, Shimak RM, et al. Neutralizing monoclonal antibodies block Chikungunya virus entry and release by targeting an epitope critical to viral pathogenesis. Cell Rep. 2015;13:2553–64.
  6. Enfissi A, Codrington J, Roosblad J, Kazanji M, Rousset D. Zika virus genome from the Americas. Lancet. 2016;387:227.

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