Evidence map›Paper›PMID 34353481›Full record

ReviewAdvances in virus research2021

A holistic perspective on herpes simplex virus (HSV) ecology and evolution.

Molly M Rathbun, Moriah L Szpara

Open access · greenAbstract readReview
In one paragraph

Review in Advances in virus research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
42.5field-weighted citation impact, top 1% of its field
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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 47 citations in OpenAlex.

  1. Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026
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  7. FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025
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4 · The record

Corrections and comments

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

2 authors at 1 institution in 1 country.

Molly M RathbunDepartment of Biochemistry and Molecular Biology, Department of Biology, Center for Infectious Disease Dynamics, and Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, PA, United States.
Moriah L SzparaDepartment of Biochemistry and Molecular Biology, Department of Biology, Center for Infectious Disease Dynamics, and Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, PA, United States. Electronic address: moriah@psu.edu.
Pennsylvania State University · US

Funding

Computation, Bioinformatics, and Statistics (CBIOS) Training ProgramT32GM102057 · NIGMS · PENNSYLVANIA STATE UNIVERSITY, THE · PI CHIAROMONTE, FRANCESCA, GIRIRAJAN, SANTHOSH · 2013 to 2022
$2.7M
Forward genetic prediction and testing of virulence loci in herpes simplex virus 1R01AI132692 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI SZPARA, MORIAH · 2018 to 2022
$2.3M
Genomic analysis of HSV-1 in the niche of genital infectionR21AI130676 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI SZPARA, MORIAH · 2017 to 2018
$439k
NIAID NIH HHS R01 AI132692NIAID NIH HHS R21 AI130676NIGMS NIH HHS T32 GM102057
6 · The paper itself

Abstract

Herpes simplex viruses (HSV) cause chronic infection in humans that are characterized by periodic episodes of mucosal shedding and ulcerative disease. HSV causes millions of infections world-wide, with lifelong bouts of viral reactivation from latency in neuronal ganglia. Infected individuals experience different levels of disease severity and frequency of reactivation. There are two distantly related HSV species, with HSV-1 infections historically found most often in the oral niche and HSV-2 infections in the genital niche. Over the last two decades, HSV-1 has emerged as the leading cause of first-episode genital herpes in multiple countries. While HSV-1 has the highest level of genetic diversity among human alpha-herpesviruses, it is not yet known how quickly the HSV-1 viral population in a human host adapts over time, or if there are population bottlenecks associated with viral reactivation and/or transmission. It is also unknown how the ecological environments in which HSV infections occur influence their evolutionary trajectory, or that of co-occurring viruses and microbes. In this review, we explore how HSV accrues genetic diversity within each new infection, and yet maintains its ability to successfully infect most of the human population. A holistic examination of the ecological context of natural human infections can expand our awareness of how HSV adapts as it moves within and between human hosts, and reveal the complexity of these lifelong human-virus interactions. These insights may in turn suggest new areas of exploration for other chronic pathogens that successfully evolve and persist among their hosts.

Indexed as

Herpesvirus 1, HumanVirus LatencyGangliaHumansNeuronsClinical genomicsHerpesvirusHSV-1Virus ecologyVirus evolution

Identifiers

PMID34353481
PMCPMC8943685
OpenAlexW3188668354

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.