Abstract
Background: HTLV-1/2 mother-to-child transmission (MTCT) is an important route for the maintenance of HTLV-1/2 within populations and disproportionally contributes to the burden of HTLV-1-associated diseases. Avoidance of breastfeeding is the safest recommendation to prevent MTCT. Due to the benefits of breastfeeding, alternative methods that would allow seropositive mothers to breastfeed their babies are needed. There is limited knowledge about HTLV-1/2 infection and breastmilk. Methods: Paired blood and milk samples collected from HTLV-1/2 seropositive mothers were tested for HTLV-1 proviral load (PVL) quantification and for the detection of anti-HTLV-1/2 IgG. Results: All breastmilk samples had detectable anti-HTLV-1/2 IgG. HTLV-1/2 proviral DNA was detected in all samples except for one. HTLV-1 PVL and IgG binding ratio (BR) was similar in milk and plasma. However, antibody titer was significantly higher in blood (Median (95%CI): Milk:128 (32–512); Plasma:131,584 (16,000–131,584), p < 0.05). There was a strong correlation between HTLV-1 PVL, anti-HTLV-1/2 IgG BR, and titer when comparing milk and blood. PVL did not correlate with antibody BR nor titer in blood or milk. Conclusions: Anti-HTLV-1/2 IgG are present in milk in the same proportion as blood but in lower quantity. PVL in milk correlates with blood.
Highlights
Human T-cell lymphotropic virus (HTLV) infects at least 5–10 million individuals in the world [1]
HTLV-1 causes a range of diseases, including a severe leukaemia, called adult T-cell leukaemia/lymphoma (ATLL), and a debilitating and progressive neurological disease known as HTLV-1-associated myelopathy (HAM)
There was no significant difference between the binding ratio (BR) of anti-HTLV-1/2 IgG between blood plasma and breast milk supernatant (Median (95%CI): Milk: 5.9 (2.5–16.6); Plasma: 5.7 (2.8–14.4), p > 0.05)
Summary
Human T-cell lymphotropic virus (HTLV) infects at least 5–10 million individuals in the world [1]. HTLV-1 causes a range of diseases, including a severe leukaemia, called adult T-cell leukaemia/lymphoma (ATLL), and a debilitating and progressive neurological disease known as HTLV-1-associated myelopathy (HAM). It is becoming increasingly evident that the impact of HTLV-1 is wider still and a multitude of inflammatory conditions including uveitis, infective dermatitis, and lung inflammation may be caused by this virus [2] and this may, in part, explain the 57% increase in the adjusted mortality rate associated with HTLV-1 infection [2]. HTLV-2 is rarely associated with disease and is less prevalent than HTLV-1. These retroviruses maintain life-long infection mainly by clonal expansion of infected cells. Virions are rarely produced in stable chronic infection [3]
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