A small subset of patients infected with Borrelia burgdorferi (Bb) does not produce Bb specific antibody. Our research provides additional evidence of a genetic predisposition for seronegativity in some individuals with Lyme disease. Because human leukocyte antigen (HLA) class II, a heterodimeric glycoprotein, plays an essential role in the regulation of antibody production, we investigated the difference in HLA genes between seropositive and seronegative patients with Lyme disease (LD). Our results show that HLA-DR7 was associated with anti-Bb antibody production. Nine out of the 22 seropositive LD patients (40.9%) had HLA-DRB1*0701, *0703, *0704 (HLA-DR7); only 1 out of the 18 seronegative LD patients (5.6%) had HLA-DR7 (odds ratio (OR)=11.8, P=0.0126). HLA-DRB1*01021 and HLA-DRB1*0101, *0104, *0105 (HLA-DR1) contributed negatively to anti-Bb antibody production. Seven of 18 seronegative LD patients had HLA-DR1, only 1 of 22 seropositive LD patients had HLA-DR1 (38.9% vs. 4.5%, OR=13.4, P=0.0138). These results suggest that the presence and or lack of production of specific antibody to Bb infection may be associated with particular HLA specificities of the Class II.
14 years undiagnosed Lyme. I had a bulls-eye rash following a camping trip to NC in 1994. Swollen knees and replapsing and remitting vertigo followed for the next 14 years. All Lyme tests negative. Could possibly be B. lonestari due to being bit in the South.
Just began treatment with low dose Minocycline and Benicar.