Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors.
Jun Arii *Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan. jarii@med.kobe-u.ac.jp.ORCID 0000-0002-1689-4016
Salma Aktar *Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID 0000-0001-5602-1909
Jing Rin HuangDivision of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Mansaku HiraiDivision of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID 0009-0001-3639-9194
Yoshiki KawamuraDepartment of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.ORCID 0000-0003-3942-7098
Hiroki MiuraDepartment of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.
Bochao WangDivision of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Satoshi NagamataDivision of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Mitsuhiro NishimuraDivision of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Tetsushi YoshikawaDepartment of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.
Reuben S HarrisDepartment of Biochemistry and Structural Biology, University of Texas San Antonio, San Antonio, TX, USA.ORCID 0000-0002-9034-9112
Yasuko MoriDivision of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID 0000-0002-6595-8522
Funding
APOBEC3 Proteins in HIV RestrictionR37AI064046 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HARRIS, REUBEN S · 2015 to 2024
$4.2M
Japan Agency for Medical Research and Development (AMED) 20wm0325005hJapan Agency for Medical Research and Development (AMED) 22gm6410022hMEXT | Japan Science and Technology Agency (JST) SPRING (JPMJSP2148)MEXT | Japan Society for the Promotion of Science (JSPS) 20H03496MEXT | Japan Society for the Promotion of Science (JSPS) 23K18589Ministry of Education, Culture, Sports, Science and Technology (MEXT) Leading Initiative for Excellent Young Researchers GrantNIAID NIH HHS R37 AI064046U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI064046
6 · The paper itself
Abstract
Human herpesviruses exhibit diverse pathogenic outcomes and the molecular reasons are not fully understood. Human herpesvirus 6B (HHV-6B) causes exanthema subitum and encephalitis, whereas the closely related HHV-6A is typically asymptomatic. Here, we show that cellular APOBEC3 enzymes restrict HHV-6A replication but not HHV-6B. HHV-6B expresses higher levels of the U28 protein, which binds multiple APOBEC3 proteins and promotes their relocalization and degradation. In contrast, HHV-6A fails to counteract APOBEC3 activity and accumulates extensive mutations in both cell- and patient-derived viral genomes. Individual APOBEC3 gene ablation enhances HHV-6A replication and reduces the viral mutation burden. Together, our studies suggest that differential susceptibility to APOBEC3 restriction may help to shape the evolvability and clinical manifestations of HHV-6A and HHV-6B.
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.
A viral APOBEC3 antagonist distinguishes HHV-6A from HHV-6B. · full record | OpenQuestion