ReviewGene2022
Human T-lymphotropic virus type 1 and novel coronavirus disease 2019; More complex than just a simple coinfection.
Review in Gene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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.
Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Immune response to COVID-19 vaccines among people living with human T-cell lymphotropic virus type 1 infection: a retrospective cohort study from Iran.Journal of neurovirology · 2025Article
- A novel hybrid method with convergence analysis for approximation of HTLV-I dynamics model.Scientific reports · 2024Article
- Association between HTLV-1/2 infection and COVID-19 severity in a migrant Shipibo-Konibo population in Lima, Peru.PLOS global public health · 2024Article
- COVID-19 among People Living with HTLV-1 Infection in Rio de Janeiro, Brazil.Pathogens (Basel, Switzerland) · 2023Article
- Bioinformatic and systems biology approach revealing the shared genes and molecular mechanisms between COVID-19 and non-alcoholic hepatitis.Frontiers in molecular biosciences · 2023Article
- Seroepidemiology of HBV, HCV, HIV, HTLV, and CMV in Pregnant Women Referring to Sari Birth Cohort.Advanced biomedical research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The recent coronavirus disease 2019 (COVID-19) significantly affected many people worldwide, especially those with underlying diseases. While some people with underlying illnesses, including cardiovascular diseases, are more vulnerable to develop severe COVID-19, other populations, including people who have autoimmune diseases, may develop severe diseases similar to the general population. The severity and outcome of COVID-19 are reviewed in individuals with underlying viral diseases, including acquired immune deficiency syndrome and hepatitis, however, some infectious diseases, including human T-lymphotropic virus type 1 (HTLV-1) diseases, is under-reported in the literature. HTLV-1 is a sexually transmitted disease that is endemic in some parts of the world. Infected patients may develop clinical symptoms of HTLV-1 associated myelopathy / tropical spastic paraparesis (HAM/TSP) and adult T cell leukemia (ATL) or may remain asymptomatic during their life. To the best of our knowledge, no clinical studies evaluate the severity and outcomes of SARS-CoV-2 infection in HTLV-1 infected patients. We aimed to review the pathogenesis of both of these viral infections and discuss their similarities in provoking immune responses. Although HTLV-1 infected patients may have had variable degrees of inflammation and immune system dysregulation, the available data is limited to conclude that HTLV-1 infected patients may be more vulnerable to developing severe COVID-19 in contrast to the general population.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.