Xiaohan Yang1, Yuanyuan Li2, Changbin Zhang1, Wenli Zhan1, Jia Xie3, Siqi Hu3, Huiying Chai1, Pan Liu1, Hongyu Zhao1, Bin Tang1, Keyi Chen1, Jian Yu4, Aihua Yin1, Mingyong Luo5. 1. Medical Genetic Centre, Guangdong Women and Children Hospital, Guangzhou, China; Medical Genetic Centre, Guangdong Women and Children Hospital, Guangzhou Medical University, Guangzhou, China. 2. State Key Laboratory of Respiratory Disease, National Clinical Researh Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China; Nanshan Medicine Innovation Institute of Guangdong Province, Guangzhou, China. 3. Medical Genetic Centre, Guangdong Women and Children Hospital, Guangzhou Medical University, Guangzhou, China. 4. Beijing Advanced Innovation Center for Biomedical Engineering, Beihang University, Beijing, China; School of Biological Science and Medical Engineering, Beihang University, Beijing, China. 5. Medical Genetic Centre, Guangdong Women and Children Hospital, Guangzhou, China; Medical Genetic Centre, Guangdong Women and Children Hospital, Guangzhou Medical University, Guangzhou, China. Electronic address: luo-my@163.com.
Abstract
BACKGROUND: Coxsackievirus A6 (CA6) infection may lead to high hand-foot-and-mouth disease (HFMD) aggregation in children. We aimed to analyze the clinical and phylogenetic features of severe CA6-associated pediatric HFMD. METHODS: The clinical and laboratory features of 206 and 55 children with mild and severe CA6-associated HFMD, respectively, were summarized. The CA6 phylogenetic tree was depicted using combinatorial analysis of the VP1-encoding regions and neighbor-joining method. RESULTS: CA6 was the major pathogen both in mild and severe HFMD in 2017. Most CA6-associated severe HFMD cases showed high fever, skin rash, age younger than 36 months, and elevated white blood cell and C-reactive protein levels, and there were no significant differences compared to the mild cases (p > 0.05). The severe cases were significantly more likely (p < 0.05) to show male sex, long fever duration, decreased oral intake, tonsil enlargement, diarrhea, vomiting, elevated levels of creatine kinase and blood glucose, and positive fecal occult-blood test results. Severe complications included aseptic meningitis (29/55, 52.7%) and pulmonary edema (6/55, 10.9%) were observed in severe cases. Furthermore, genetic analyses showed all CA6 isolates belonged to lineage E2, and two amino acid changes of V174I and T283A in VP1 may be associated with the severity of HFMD. CONCLUSIONS: CA6 has become a major cause of HFMD with severe systemic disorders. V174I and T283A of VP1 may be associated with the severity of CA6 infection. These findings could raise awareness of the clinical importance of CA6 infection among practitioners.
BACKGROUND:Coxsackievirus A6 (CA6) infection may lead to high hand-foot-and-mouth disease (HFMD) aggregation in children. We aimed to analyze the clinical and phylogenetic features of severe CA6-associated pediatric HFMD. METHODS: The clinical and laboratory features of 206 and 55 children with mild and severe CA6-associated HFMD, respectively, were summarized. The CA6 phylogenetic tree was depicted using combinatorial analysis of the VP1-encoding regions and neighbor-joining method. RESULTS: CA6 was the major pathogen both in mild and severe HFMD in 2017. Most CA6-associated severe HFMD cases showed high fever, skin rash, age younger than 36 months, and elevated white blood cell and C-reactive protein levels, and there were no significant differences compared to the mild cases (p > 0.05). The severe cases were significantly more likely (p < 0.05) to show male sex, long fever duration, decreased oral intake, tonsil enlargement, diarrhea, vomiting, elevated levels of creatine kinase and blood glucose, and positive fecal occult-blood test results. Severe complications included aseptic meningitis (29/55, 52.7%) and pulmonary edema (6/55, 10.9%) were observed in severe cases. Furthermore, genetic analyses showed all CA6 isolates belonged to lineage E2, and two amino acid changes of V174I and T283A in VP1 may be associated with the severity of HFMD. CONCLUSIONS: CA6 has become a major cause of HFMD with severe systemic disorders. V174I and T283A of VP1 may be associated with the severity of CA6 infection. These findings could raise awareness of the clinical importance of CA6 infection among practitioners.
Authors: Adriana Luchs; Lais Sampaio de Azevedo; Ellen Viana de Souza; Roberta Salzone Medeiros; Yasmin França Viana Pires de Souza; Dalane Loudal Florentino Teixeira; Thiago Franco de Oliveira Carneiro; Gabriela Maria Fernandes de Alencar; Fernanda Lúcia de Sousa Leite Morais; Diana de Fátima Alves Pinto; Thelma Suely Okay; Lidia Yamamoto; Vanessa Dos Santos Morais; Emerson Luiz Lima Araújo; Elcio Leal; Antonio Charlys da Costa Journal: Rev Inst Med Trop Sao Paulo Date: 2022-02-21 Impact factor: 1.846
Authors: Stefania Leuci; Noemi Coppola; Tiziana Cantile; Elena Calabria; Laurenta Lelia Mihai; Michele Davide Mignogna Journal: Int J Environ Res Public Health Date: 2022-03-25 Impact factor: 3.390