Evidence map›Paper›PMID 33653890›Full record

ArticlemBio2021

Contributions of the Four Essential Entry Glycoproteins to HSV-1 Tropism and the Selection of Entry Routes.

Adam T Hilterbrand, Raecliffe E Daly, Ekaterina E Heldwein

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Anti-Herpes Simplex Virus Type 1 Activity ofInternational journal of molecular sciences · 2025
    Article
  9. The Procaine-Based ProcClusterInternational journal of molecular sciences · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Molecular Engineering of Virus Tropism.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Adam T HilterbrandDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, USA.ORCID 0000-0003-4221-6523
Raecliffe E DalyDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, USA.
Ekaterina E HeldweinDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, USA katya.heldwein@tufts.edu.ORCID 0000-0003-3113-6958
Tufts University · US

Funding

Infectious Disease Training-Pathogenesis/Host ResponseT32AI007329 · NIAID · TUFTS MEDICAL CENTER · PI HU, LINDEN T · 1988 to 2018
$4.1M
Dissection of HSV-1 entry mechanisms using VSV pseudotype platformR21AI140711 · NIAID · TUFTS UNIVERSITY BOSTON · PI HELDWEIN, EKATERINA · 2018 to 2019
$454k
Howard Hughes Medical Institute 55108533NIAID NIH HHS R21 AI140711NIAID NIH HHS T32 AI007329
6 · The paper itself

Abstract

Herpes simplex viruses (HSV-1 and HSV-2) encode up to 16 envelope proteins, four of which are essential for entry. However, whether these four proteins alone are sufficient to dictate the broad cellular tropism of HSV-1 and the selection of different cell type-dependent entry routes is unknown. To begin addressing this, we previously pseudotyped vesicular stomatitis virus (VSV), lacking its native glycoprotein G, with only the four essential entry glycoproteins of HSV-1: gB, gH, gL, and gD. This novel VSVΔG-BHLD pseudotype recapitulated several important features of HSV-1 entry: the requirement for gB, gH, gL, gD, and a cellular receptor and sensitivity to anti-gB and anti-gH/gL neutralizing antibodies. However, due to the use of a single cell type in that study, the tropism of the VSVΔG-BHLD pseudotype was not investigated. Here, we show that the cellular tropism of the pseudotype is severely limited compared to that of wild-type HSV-1 and that its entry pathways differ from the native HSV-1 entry pathways. To test the hypothesis that other HSV-1 envelope proteins may contribute to HSV-1 tropism, we generated a derivative pseudotype containing the HSV-1 glycoprotein C (VSVΔG-BHLD-gC) and observed a gC-dependent increase in entry efficiency in two cell types. We propose that the pseudotyping platform developed here has the potential to uncover functional contributions of HSV-1 envelope proteins to entry in a gain-of-function manner.

Indexed as

Viral TropismVirus InternalizationAnimalsCell LineChlorocebus aethiopsGain of Function MutationHEK293 CellsHeLa CellsHerpesvirus 1, HumanHumansMolecular TypingVero CellsViral Envelope Proteinsglycoprotein gC, herpes simplex virus type 1Viral Envelope Proteinscell entryendocytosisglycoproteinsherpes simplex virusesHSV-1inhibitorspseudotypes

Identifiers

PMID33653890
PMCPMC8092210
OpenAlexW3133802713

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.