Emergence of Coxsackievirus A16 Causing Childhood Hand, Foot, and Mouth Disease: First Molecular Evidence from Bangladesh

Author:

Hoque Sheikh Ariful1ORCID,Anwar Kazi Selim2,Khan Md. Azraf Hossain3,Sultana Ummay Nasrin1,Ali Md. Ahasan4,Hossain Tania1,Sharmin Laila Shamima3,Kabir ARM Luthful2,Mollah Md. Abid Hossain5,Hoque Sk. Azimul6,Khan Masuma2,Pham Ngan Thi Kim7,Khamrin Pattara8,Okitsu Shoko7,Hayakawa Satoshi7,Ushijima Hiroshi7

Affiliation:

1. Cell and Tissue Culture Laboratory, Centre for Advanced Research in Sciences (CARS), University of Dhaka, Dhaka, Bangladesh

2. Research Division, Ad-din Women's Medical College, Dhaka, Bangladesh

3. Rajshahi Medical College Hospital, Rajshahi, Bangladesh

4. Microbiology Division, Institute of Public Health, Mohakhali, Dhaka, Bangladesh

5. Department of Pediatrics, BIRDEM-2, Shegun Bagicha, Dhaka, Bangladesh

6. Department of Pediatrics, National Institute Neuroscience and Hospital, Dhaka, Bangladesh

7. Division of Microbiology, Department of Pathology and Microbiology, School of Medicine, Nihon University, Tokyo, Japan

8. Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand

Abstract

Abstract Objective Hand, foot, and mouth disease (HFMD), caused by various human enteroviruses (EVs), has emerged in the children of Bangladesh in recent years. However, the etiological agents of HFMD in Bangladeshi children are not yet elucidated. This study aimed to investigate the causative agents with molecular characterization. Methods Viral RNAs were detected from the blister fluid samples by reverse transcription polymerase chain reaction; genotyping was done by sequence-based analysis of the partial viral capsid protein 1 (VP1) region, and the evolutionary relationships among the genotypes were investigated by phylogenetic analysis. Results EV-RNAs were identified in 14 (61%) blister fluid samples out of 23 children who were suspected of HFMD during an outbreak in Rajshahi in 2020. Genome sequence analysis of the VP1 gene was performed on four strains: all the four were coxsackievirus A16 (CVA16) that clustered in B1c subgenotype. These strains showed 95 to 98% nucleotide identity with those reported in India in 2013/2018. Conclusion After our first report on clinical evidence of childhood HFMD in Bangladesh, this time, we provided laboratory confirmation of the emergence of CVA16 as a causative agent of HFMD in Bangladeshi children. There is an urgent need for nationwide, in-depth, clinicoepidemiological surveillance on HFMD including its virology and genetics before it becomes endemic in Bangladesh.

Funder

University of Dhaka

Publisher

Georg Thieme Verlag KG

Subject

Infectious Diseases,Pediatrics, Perinatology and Child Health

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