ArticleJournal of virology2021
Skeletal Muscle Is an Early Site of Zika Virus Replication and Injury, Which Impairs Myogenesis.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Enterovirus 71 drives TLR2-NF-κB-dependent inflammatory skeletal muscle injury in neonatal BALB/c mice.Microbiology spectrum · 2026Article
- Bioactive Flavanone Glycoside Isolated from Leaves ofACS omega · 2025Article
- Zika virus infection disturbs development of human muscle progenitor cells.Frontiers in cellular and infection microbiology · 2025Article
- Chikungunya and Mayaro Viruses Induce Chronic Skeletal Muscle Atrophy Triggered by Pro-Inflammatory and Oxidative Response.International journal of molecular sciences · 2024Article
- Immunosuppression-induced Zika virus reactivation causes brain inflammation and behavioral deficits in mice.iScience · 2024Article
- Skin muscle is the initial site of viral replication for arboviral bunyavirus infection.Nature communications · 2024Article
- Morphological and functional cardiac alterations in children with congenital Zika syndrome and severe neurological deficits.PLoS neglected tropical diseases · 2023Article
- Impaired muscle stem cell function and abnormal myogenesis in acquired myopathies.Bioscience reports · 2023Review
- The regenerative potential of Pax3/Pax7 on skeletal muscle injury.Journal, genetic engineering & biotechnology · 2022Review
- Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Zika virus (ZIKV) infection became a worldwide concern due to its correlation with the development of microcephaly and other neurological disorders. ZIKV neurotropism is well characterized, but the role of peripheral viral amplification to brain infection remains unknown. Here, we found that ZIKV replicates in human primary skeletal muscle myoblasts, impairing its differentiation into myotubes but not interfering with the integrity of the already-formed muscle fibers. Using mouse models, we showed ZIKV tropism to muscle tissue either during embryogenesis after maternal transmission or when infection occurred after birth. Interestingly, ZIKV replication in the mouse skeletal muscle started immediately after ZIKV inoculation, preceding viral RNA detection in the brain and causing no disruption to the integrity of the blood brain barrier, and remained active for more than 2 weeks, whereas replication in the spleen and liver were not sustained over time. In addition, ZIKV infection of the skeletal muscle induces necrotic lesions, inflammation, and fiber atrophy. We also found a reduction in the expression of regulatory myogenic factors that are essential for muscle repair after injury. Taken together, our results indicate that the skeletal muscle is an early site of viral amplification and lesion that may result in late consequences in muscle development after ZIKV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.