Vertical mother‐to‐infant transmission of herpes simplex virus 2 is correlated with tropism due to mutations in viral UL13

Author:

Shiraki Kimiyasu12,Daikoku Tohru3,Prichard Mark N.4,Matsuo Koma5,Okuda Tomoko2,Yoshida Yoshihiro2,Takemoto Masaya3,Takeuchi Kenji6,Sada Kiyonao6,Whitley Richard4,Kawana Takashi7

Affiliation:

1. Department of Nursing Senri Kinran University, Suita Suita Osaka Japan

2. Department of Virology, Graduate School of Medicine and Pharmaceutical Sciences University of Toyama Toyama Toyama Japan

3. Department of Microbiology, Faculty of Pharmaceutical Sciences Hokuriku University Kanazawa Ishikawa Japan

4. Department of Pediatrics, Heersink School of Medicine University of Alabama at Birmingham Birmingham Alabama USA

5. Department of Dermatology The Jikei University School of Medicine Tokyo Japan

6. Department of Genome Science and Microbiology, Faculty of Medical Sciences University of Fukui Eiheiji Fukui Japan

7. Department of Obstetrics and Gynecology Teikyo University Mizonokuchi Hospital Kawasaki Kanagawa Japan

Abstract

AbstractAlthough neonates are commonly exposed to vaginal herpes simplex virus (HSV)‐2, neonatal herpes is rare. Therefore, we analyzed paired infant and maternal HSV‐2 isolates from two cases of mother‐to‐infant transmission to identify viral factors contributing to vertical transmission. Sixteen infant isolates with neonatal herpes and 27 genital isolates in their third trimester were included. The infant isolates were significantly more temperature‐independent than the maternal isolates. Sequence comparison revealed viral UL13 protein kinase (UL13‐PK) mutation in the infant isolates in both cases. In the expanded cohort, infant isolates (5/18) had significantly more UL13‐PK mutations than genital isolates (1/29). Isolates within 8 days post‐birth (3/4) had a significantly higher frequency of UL13‐PK mutation than those after 9 days (2/14), suggesting a close association between UL13‐PK mutations and vertical transmission. Elongation factor 1‐delta was identified as a target of UL13‐PK by proteomic analysis of UL13‐PK‐positive and ‐negative HepG2 cells. The mixed infant isolates with the intact and mutated UL13‐PK conferred altered cell tropism, temperature independence adapting to fetal temperature, and better growth properties in Vero and hepatoblastoma HepG2 cells than in HSV‐2 with intact and mutated UL13‐PK alone, indicating that viral UL13‐PK mutation is essential for vertical HSV‐2 transmission.

Publisher

Wiley

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