Abstract
The human T-cell leukaemia virus type 1 (HTLV-1) is associated with pulmonary inflammation. Indigenous Australians in central Australia have a very high prevalence of HTLV-1 infection and we hypothesised that this might contribute to high rates of bronchiectasis in this population.
80 Indigenous adults with confirmed bronchiectasis, each matched by age, sex and language to two controls without bronchiectasis, were recruited. Case notes and chest imaging were reviewed, HTLV-1 serology and the number of peripheral blood leukocytes (PBLs) infected with HTLV-1 (pro-viral load (PVL)) were determined, and radiological abnormality scores were calculated. Participants were followed for a mean±sd of 1.14±0.86 years and causes of death were determined.
Median (interquartile range) HTLV-1 PVL for cases was 8-fold higher than controls (cases 213.8 (19.7–3776.3) copies per 105 PBLs versus controls 26.6 (0.9–361) copies per 105 PBLs; p=0.002). Radiological abnormality scores were higher for cases with HTLV-1 PVL ≥1000 copies per 105 PBLs and no cause of bronchiectasis other than HTLV-1 infection. Major predictors of bronchiectasis were prior severe lower respiratory tract infection (adjusted OR (aOR) 17.83, 95% CI 4.51–70.49; p<0.001) and an HTLV-1 PVL ≥1000 copies per 105 PBLs (aOR 12.41, 95% CI 3.84–40.15; p<0.001). Bronchiectasis (aOR 4.27, 95% CI 2.04–8.94; p<0.001) and HTLV-1 PVL ≥1000 copies per 105 PBLs (aOR 3.69, 95% CI 1.11–12.27; p=0.033) predicted death.
High HTLV-1 PVLs are associated with bronchiectasis and with more extensive radiological abnormalities, which may result from HTLV-1-mediated airway inflammation.
Abstract
Higher numbers of HTLV-1-infected cells in peripheral blood are associated with bronchiectasis and more extensive radiological abnormalities among those with no cause for bronchiectasis other than HTLV-1 infection http://bit.ly/2V6pw98
Footnotes
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Conflict of interest: L. Einsiedel has nothing to disclose.
Conflict of interest: H. Pham has nothing to disclose.
Conflict of interest: V. Au has nothing to disclose.
Conflict of interest: S. Hatami has nothing to disclose.
Conflict of interest: K. Wilson has nothing to disclose.
Conflict of interest: T. Spelman has nothing to disclose.
Conflict of interest: H. Jersmann has nothing to disclose.
Support statement: This study received funding from the National Health and Medical Research Council of Australia (NHMRC project grant 1012945). Funding information for this article has been deposited with the Crossref Funder Registry.
- Received January 4, 2019.
- Accepted September 14, 2019.
- Copyright ©ERS 2019
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