Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Virus inactivation in a proportion of human T-cell leukaemia virus type I-infected T-cell clones arises through naturally occurring mutations.

The Journal of general virology - 1 Jan 2000

Rose N J, Richardson J H, Desselberger U, Lever A M

Abstract excerpt

Human T-cell leukaemia virus type I (HTLV-I) is the aetiological agent of adult T-cell leukaemia/lymphoma and tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM). The trans-activating protein (Tax) of HTLV-I is strongly implicated in cellular proliferation. We examined the tax gene and 5' long terminal repeat (LTR) sequences in eight naturally infected T-cell clones derived from TSP/HAM-affected...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to 5' Untranslated Regions
Share to Clone Cells

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Enhancer Elements, Genetic

Share to Gene Products, tax

Share to HTLV-I Infections

Share to Human T-lymphotropic virus 1

Share to Terminal Repeat Sequences

Share to Virus Activation

Source

Identifiers

PMID: 10640546
DOI: 10.1099/0022-1317-81-1-97

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Virus inactivation in a proportion of human T-cell leukaemia virus type I-infected T-cell clones arises through naturally occurring mutations.PMID 10640546Read ↗

Somatic mutation in human T-cell leukemia virus type 1 provirus and flanking cellular sequences during clonal expansion in vivo.Semantic proximity Read ↗

Mutation rates in LTR of HTLV-1 in HAM/TSP patients and the carriers are similarly high to Tax/Rex-coding sequence.Semantic proximity Read ↗

Variable immortalizing potential and frequent virus latency in blood-derived T-cell clones infected with human T-cell leukemia virus type I.Semantic proximity Read ↗

HTLV-1 intragenic viral enhancer influences immortalization phenotype in vitro, but is dispensable for persistence and disease development in animal models.Semantic proximity Read ↗

Clonal expansion of HTLV-1 infected cells depends on the CD4 versus CD8 phenotype.Semantic proximity Read ↗

Clonal expansion of infected cells: a way of life for HTLV-I.Semantic proximity Read ↗

Clonal expansion of human T-cell leukemia virus type I-infected cells in asymptomatic and symptomatic carriers without malignancy.Semantic proximity Read ↗

APOBEC3G generates nonsense mutations in human T-cell leukemia virus type 1 proviral genomes in vivo.Semantic proximity Read ↗

Comparative molecular analysis of HTLV-I proviral DNA in HTLV-I infected members of a family with a discordant HTLV-I-associated myelopathy in monozygotic twins.Semantic proximity Read ↗

The transactivator gene of human T-cell leukemia virus type I is more variable within and between healthy carriers than patients with tropical spastic paraparesis.Semantic proximity Read ↗

Single-cell heterogeneity and cell-cycle-related viral gene bursts in the human leukaemia virus HTLV-1Semantic proximity Read ↗

Human T cell leukemia virus type I (HTLV-I) molecular genotypes and disease outcome.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.