03397nas a2200385   4500000000100000008004100001260001200042653001600054653002800070653003100098653001200129653002600141653001200167653002700179653005600206100001200262700002100274700001900295700001300314700001600327700001500343700002000358700001800378700001500396700001400411700001400425700001200439700002600451245015300477856008100630300001100711490000700722520226800729022001402997       2020                            d  c01/202010aHepatitis B10acomplement 3b receptors10acomplement system proteins10aficolin10agenetic polymorphisms10aleprosy10amannose-binding lectin10amannose-binding protein-associated serine proteases1 aBoldt A1 aOliveira-Toré C1 aKretzschmar GC1 aMendes H1 aStinghen ST1 aAndrade FA1 aBumiller-Bini V1 aGonçalves LB1 aBraga ACDM1 aStahlke E1 aVelavan T1 aThiel S1 ade Messias-Reason IJT00aHepatitis B Virus Infection Among Leprosy Patients: A Case for Polymorphisms Compromising Activation of the Lectin Pathway and Complement Receptors.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7904891/pdf/fimmu-11-574457.pdf  a5744570 v113 a<p>Thousands of leprosy patients not only suffer from physical deformities, but also either have or have had hepatitis B virus (HBV) coinfection. Polymorphisms of the complement system modulate susceptibility to leprosy, but genetic susceptibility to past or present HBV infection is unknown. We used sequencing and multiplex sequence-specific PCR to genotype 72 polymorphisms of seven genes (, ) encoding components of the lectin pathway, and two genes encoding complement receptors () in 190 patients, of which 74 were positive for HBsAg and/or anti-HBc (HBV+, 93.2% with a resolved infection) and 116 lepromatous patients, and 408 HBV-blood donors. In addition, we tested for levels of proteins of the lectin pathway. We found no difference between serum concentrations of mannan-binding lectin (MBL), MBL-associated serine proteins (MASP-1, MASP-2, MASP-3, MAp44), ficolin-3 (FCN-3), soluble complement receptor 1 (sCR1) and MBL mediated C4 activation, measured by ELISA or TRIFMA in up to 167 HBV+ and HBV- patients. Haplotypes lowering protein levels or encoding dysfunctional proteins increased susceptibility to HBV infection:  (OR = 3.4, p = 0.02),  (OR = 4.0, p = 0.015) and  (OR = 5.4, p = 0.03). Conversely,  haplotype, associated with higher gene expression, was protective (OR = 0.56, P = 0.033). Other haplotypes associated with HBV susceptibility were:  (OR = 19.25, P = 0.003),  (OR = 2.65, P = 0.011) and  (OR = 12.55, P = 0.014). Some polymorphisms in ficolin genes associated with lower protein levels increased susceptibility to leprosy/HBV infection:  (OR = 1.66, P = 0.029),  (OR = 6.73, P = 0.008), and  (OR = 12.54, P = 0.037), and to lepromatous disease/HBV infection:  (OR = 2.5, P = 0.009), whereas  was associated with increased FCN-2 expression and resistance against coinfection (OR = 0.29, P = 0.026). These associations were independent of demographic factors and did not increase susceptibility to leprosy , except . Associations for , and  variants were also independent of each other. In conclusion, polymorphisms compromising activation of the lectin pathway of complement increase susceptibility to HBV infection, with ficolin polymorphisms playing a major role in modulating the susceptibility among leprosy patients.</p>  a1664-3224