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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 ( MBL2 ,  FCN1, FCN2, FCN3, MASP1, MASP2, C3 ) encoding components of the lectin pathway, and two genes encoding complement receptors ( CR1, VSIG4 ) 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:  MBL2*LYQC  (OR = 3.4, p = 0.02),  MASP1*AC_CC  (OR = 4.0, p = 0.015) and  MASP2*1C2-l  (OR = 5.4, p = 0.03). Conversely,  FCN1*3C2  haplotype, associated with higher gene expression, was protective (OR = 0.56, P = 0.033). Other haplotypes associated with HBV susceptibility were:  MASP2*2B1-i  (OR = 19.25, P = 0.003),  CR1*3A  (OR = 2.65, P = 0.011) and  VSIG4*TGGRCG  (OR = 12.55, P = 0.014). Some polymorphisms in ficolin genes associated with lower protein levels increased susceptibility to leprosy/HBV infection:  FCN*1  (OR = 1.66, P = 0.029),  FCN2*GGGCAC  (OR = 6.73, P = 0.008), and  FCN3*del_del_C  (OR = 12.54, P = 0.037), and to lepromatous disease/HBV infection:  FCN2*TA  (OR = 2.5, P = 0.009), whereas  FCN2*MAG  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  per se , except  MASP2*1C2-l . Associations for  FCN2, FCN3, MASP1, MASP2 , and  VSIG4  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.

Hepatitis B Virus Infection Among Leprosy Patients: A Case for Polymorphisms Compromising Activation of the Lectin Pathway and Complement Receptors