Evidence map›Paper›PMID 37896833›Full record

ArticleViruses2023

Human Mannose Receptor 1 Attenuates HIV-1 Infectivity in a Virus Isolate-Specific Manner.

Hideki Saito, Sayaka Sukegawa, Sandra Kao, Klaus Strebel

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2023. 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
0.3field-weighted citation impact, top 45% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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

4 authors at 2 institutions in 2 countries.

Hideki SaitoViral Biochemistry Section, Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, MD 20892, USA.
Sayaka SukegawaViral Biochemistry Section, Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, MD 20892, USA.
Sandra KaoViral Biochemistry Section, Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, MD 20892, USA.
Klaus StrebelViral Biochemistry Section, Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, MD 20892, USA.ORCID 0000-0002-2827-8923
National Institutes of Health · USTokyo Medical and Dental University · JP

Funding

Molecular Analysis Of Retroviral Genes And Their ProductsZIAAI000669 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STREBEL, KLAUS · 2009 to 2025
$25.2M
Molecular Analysis Of Retroviral Genes &Their ProductsZ01AI000669 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI STREBEL, KLAUS · 1993 to 2008
$852k
Intramural NIH HHS Z01 AI000669Intramural NIH HHS ZIA AI000669
6 · The paper itself

Abstract

Human mannose receptor 1 (hMRC1) is a transmembrane glycoprotein that belongs to the C-type lectin family and is expressed on the surface of most tissue macrophages. hMRC1 contributes to the binding and transmission of HIV-1 and is involved in the endocytic uptake of HIV-1 for subsequent antigen presentation. We previously reported that hMRC1 functions as an antiviral factor by inhibiting virus release through a BST-2-like mechanism. The inhibition of virus release was not virus isolate-specific and, surprisingly, was not Env-dependent. We now report on another hMRC1 antiviral function that affects the infectivity of viral particles. Unlike its effect on virus release, the inhibition of viral infectivity by hMRC1 was virus isolate-specific. An analysis of chimeric Env revealed that the Env V3 region was a critical determinant for the inhibitory effect of hMRC1. Of note, exogenously expressed hMRC1 was packaged into viral particles in an Env-independent manner. Co-immunoprecipitation studies revealed a strong interaction of the hMRC1-sensitive NL43 Env with hMRC1, while the hMRC1-insensitive Envs of AD8 and 49.5 isolates interacted poorly if at all with hMRC1. An analysis of a panel of Transmitted/Founder (T/F) viruses revealed that all of them were R5-tropic, and more than half of them were inhibited by hMRC1. The detailed mechanism of how hMRC1 inhibits viral infectivity remains to be investigated. However, the high-affinity binding of hMRC1 to Env may cause a conformational change around the Env V3 region or obstruct the Env V3 region and may make it inaccessible for subsequent interaction with the coreceptor during virus entry.

Indexed as

HIV-1HIV InfectionsAntiviral AgentsHumansLectins, C-TypeMannose ReceptorAntiviral AgentsLectins, C-TypeMannose ReceptorHIV-1mannose receptorrestriction factorvirus assemblyvirus host interactions

Identifiers

PMID37896833
PMCPMC10612104
OpenAlexW4387407716

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.