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Tat protein may activate helper CD4+ cells in individuals infected with HIV type 1 (HIV-1). This protein is a regulatory protein that is necessary for replication of HIV-1. A study examined response of helper CD4+ T cells to recombinant (genetically engineered) Tat protein and 12 different Tat protein subunits in 15 HIV-positive individuals and 11 HIV-negative individuals (control group). HIV-positive individuals were more likely to have a response to recombinant Tat than those in the control group. Three Tat protein subunits caused a helper CD4+ T cell response in the HIV-positive individuals but not in HIV-negative individuals.

Infection with beta hemolytic streptococci may be less likely to cause rheumatic fever than other types of reactive arthritis in adults. Rheumatic fever is one type of reactive arthritis caused by this type of bacteria. A study examined 76 adults with an arthritis syndrome or increased severity of a chronic rheumatic disease. All the patients had a simultaneous rise in blood levels of antistreptolysin O (ASO). ASO is an antibody that inhibits streptolysin, a toxin produced by group A streptococci. None of the patients were diagnosed with classic rheumatic fever despite elevated blood levels of ASO. Twenty-six patients were diagnosed with arthritis in association with a known rheumatic disease, 25 with non-specific joint and muscle pain, 20 with reactive arthritis and five with septic arthritis.

A group of 151 cytomegalovirus (CMV)‐seropositive renal transplant recipients was retrospectively evaluated. CMV disease was verified in 16% of the patients 2 to 24 weeks posttransplant. The 1 year survival rates of the patients and the grafts were not impaired by CMV. Antigens in locus HLA‐B5 in the recipient and HLA‐A3 in the donor were demonstrated to be associated with an increased incidence of posttransplant CMV disease.

The association of an early steroid-resistant rejection (SRR) with HLA-DR antigens was analyzed in 410 kidney transplantations. A severe SRR leading to a poor (45) 1-year graft survival (GS) occurred in 22 transplantations (5). An acute reversible rejection (ARR) with a GS of 94 was found in 80 transplantations (20). For the 308 (75) transplantations with no early rejection episodes the GS was 91.

Gold salt therapy-induced pneumonitis is a rare complication in patients with rheumatoid arthritis (RA). We studied HLA-A, B, C, D/DR, and complement factor B (Bf) and C4 alleles in 17 patients with RA and gold-induced pneumonitis and found that these patients had strikingly homogeneous major histocompatibility complex (MHC) markers. Eight of them (47 percent) had the alleles HLA-A3 B35 Dw1 BfF C4A3,2 (BO) which were shown by family studies of some patients to be inherited as an extended MHC-haplotype with an apparent gene duplication in the C4A locus. The other high-risk phenotype, HLA-B40 with a C4 null allele, was found in eight patients (47 percent.) All but three of the 17 patients had at least one of the two high-risk markers, the frequency of these combinations being clearly higher than in the two control groups: patients with RA but with no gold-induced side effects and healthy individuals. Our study shows that use of several MHC markers together results in a strong association between the markers and the disease.

• The role of HLA and complement genes was studied in 13 patients with subacute cutaneous lupus erythematosus by combining the major histocompatibility complex class I (HLA-A, -B, and -C), class II (HLA-DR), and class III (properdin factor B [BF] and C4) phenotyping with DNA level analysis of the C4 region. Of our patients, 54% had DR2 antigens and 50% had DR3 antigens, when the frequencies in the controls were 25% and 33%, respectively. The DR3 antigen was associated with annular skin lesions that were associated with a younger age at onset, whereas the DR2 antigen was associated with papulosquamous skin lesions and an older age at onset. The frequency of C4 null alleles was 83% in the patients and 50% in the controls. The null alleles were found in both C4A and C4B loci and were not associated with any special major histocompatibility complex haplotype. The DNA studies showed that the null phenotype mostly resulted from a gene deletion. A highly increased frequency of complement C4 null alleles may be a predisposing factor for cutaneous lupus erythematosus and especially of the subacute cutaneous type.(Arch Dermatol. 1989;125:791-796)