Infection with the human T-cell leukemia virus type 1 (HTLV-1) was identified as a risk factor for bronchiectasis, and one previously unknown, among indigenous adults in central Australia, a case-controlled study reports.
In people for whom HTLV-1 was the only identifiable cause of bronchiectasis, a high number of these viruses (the viral load) were linked to the more severe lung disease.
The study, “Predictors of non-cystic fibrosis bronchiectasis in Indigenous adult residents of central Australia: results of a case–control study,” was published in the journal ERJ Open Research.
Indigenous people living in developed countries are disproportionately affected by bronchiectasis compared to each country’s general population, the study notes.
Among indigenous groups in Australia, non-cystic fibrosis bronchiectasis occurs at younger ages, affects males more than females, and overall clinical outcomes are worse than among non-indigenous people. In central Australia, in particular, a study showed that more than 1 in every 100 indigenous adults experience complications due to bronchiectasis, and that 34% of adults in this study died at an average age of 42.5.
The reason for these poor outcomes is not clear, as diseases such as tuberculosis, measles, and pertussis (whooping cough), cystic fibrosis, and immune system deficiencies are uncommon in this region.
HTLV-1 is a retrovirus found in over 40% of some central Australian communities. Most people infected with HTLV-1 live without evident symptoms, but up to 10% can develop adult T-cell leukemia and inflammatory disorders affecting the spine, lungs, and eyes.
To determine if HTLV-1 contributes to the high rates of bronchiectasis among indigenous residents of central Australia, a team of researchers at a regional center, Alice Springs Hospital, recruited a group of indigenous adults diagnosed with bronchiectasis. They conducted blood tests, image scans, and other clinical exams.
A total of 80 adult patients were selected, each matched by age, sex, and language to two indigenous adults without bronchiectasis or other lower respiratory tract infection (LRTI) who served as a control group.
Blood samples were used was to assess HTLV-1 status, along with the presence of antibodies, and markers for infections, lung conditions, and autoimmune diseases. High-resolution computed tomography (HRCT) lung scans were used to score bronchiectasis severity, and to identify such LRTIs as pneumonia.
The analysis found that adults with bronchiectasis were significantly more likely to be infected with HTLV-1 (52.5%) compared to controls (33.1%), and the median viral load (number of detected viruses) was eight times higher in patients than in controls.
HRCT scans of the lungs found a high viral load of HTLV-1 in those with significantly higher bronchiectasis scores of disease severity. In cases where bronchiectasis had an alternate cause, there were no differences in viral loads.
In 21 cases, bronchiectasis was followed by a severe lower respiratory tract infection, mostly pneumonia. Other LRTIs noted were bronchiolitis (a common viral infection), tuberculosis, and those caused by pathogens such as Streptococcus pneumoniae and adenovirus (a common virus).
A statistical analysis found the major predictors of bronchiectasis were a high HTLV-1 load, and a severe LRTI. According to the team, each 100-unit increase in the number of HTLV-1 viruses represented an increased risk of bronchiectasis by 1.07 times, and the risk was almost six times higher in those with a high viral load.
Over the course of the study, 31 patients died (38.8%) at a median age of 50, and 18 (11.3%) in the control group (median age, 58.5). Most patient deaths (90.3%, 28 out of 31) were due to complications of bronchiectasis. Of those, 43.5% had a high HTLV-1 load and 15.2% a low viral load; 19.3% did not have HTLV-1.
Based on the results, the team suggested that bronchiectasis and high viral load were predictors of mortality.
“High HTLV-1 PVLs [viral loads] are associated with bronchiectasis, and with more extensive radiological abnormalities, which may result from HTLV-1-mediated airway inflammation,” the researchers wrote.
“Notwithstanding high rates of HTLV-1 infection in central Australia, there is currently no coordinated public health strategy to reduce HTLV-1 transmission among Indigenous Australians,” they added.
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