Surveillance for Mosquitoborne Transmission of Zika Virus, New York City, NY, USA, 2016.

A large number of imported cases of Zika virus infection and the potential for transmission by Aedes albopictus mosquitoes prompted the New York City Department of Health and Mental Hygiene to conduct sentinel, enhanced passive, and syndromic surveillance for locally acquired mosquitoborne Zika virus infections in New York City, NY, USA, during June-October 2016. Suspected case-patients were those >5 years of age without a travel history or sexual exposure who had >3 compatible signs/symptoms (arthralgia, fever, conjunctivitis, or rash). We identified 15 suspected cases and tested urine samples for Zika virus by using real-time reverse transcription PCR; all results were negative.

Anti-alpha-actinin antibodies: a new marker of lupus nephritis.

The exact role of anti-ds (double stranded) DNA antibodies in the pathogenesis of kidney injury in lupus nephritis remains a focus of continuing investigation. One theory explaining the pathogenicity of anti-dsDNA antibodies in lupus nephritis is direct cross-reactivity with renal antigens. Several years ago, alpha-actinin was identified as a major cross-reactive target for pathogenic anti-dsDNA antibodies in murine SLE.

Alpha-actinin immunization elicits anti-chromatin autoimmunity in nonautoimmune mice.

Anti-dsDNA Abs are characteristic of lupus and can be found deposited in the kidneys of lupus mice. Previously, we have shown that pathogenic anti-dsDNA Abs as well as Ig eluted from the kidneys of nephritic lupus mice cross-react with alpha-actinin. Moreover, cross-reactivity with alpha-actinin characterizes nephritogenic anti-dsDNA Abs in humans with lupus as well.

Differential binding of cross-reactive anti-DNA antibodies to mesangial cells: the role of alpha-actinin.

Target Ag display is a necessary requirement for the expression of certain immune-mediated kidney diseases. We previously had shown that anti-DNA Abs that cross-react with alpha-actinin may be important in the pathogenesis of murine and human lupus nephritis; in murine models, we had found that a significant proportion of pathogenic serum and kidney-deposited Igs are alpha-actinin reactive. Furthermore, a pathogenic anti-DNA/alpha-actinin Ab showed enhanced binding to immortalized mesangial cells (MCs) derived from a lupus prone MRL-lpr/lpr mouse as compared with MCs from BALB/c mice which are not susceptible to spontaneous lupus, suggesting that kidney alpha-actinin expression may be contributing to nephritis.

BAFF overexpression and accelerated glomerular disease in mice with an incomplete genetic predisposition to systemic lupus erythematosus.

Objective: To determine whether overexpression of BAFF can accelerate the development of systemic lupus erythematosus-associated end-organ disease in hosts with an underlying autoimmune diathesis.

Methods: We introduced a BAFF transgene (Tg) into autoimmune-prone B6.Sle1 and B6.

Differential effects of interleukin-4 in peptide induced autoimmunity.

BALB/c mice immunized with multimeric DWEYSVWLSN develop IgG1 anti-DNA antibodies and glomerular immunoglobulin deposits, leading us to investigate the role of IL-4 in this model of antigen induced lupus. Splenocytes from DWEYSVWLSN immunized mice secreted IL-4 but not gamma-interferon. Following peptide immunization, IgG1 anti-peptide and anti-DNA antibodies were significantly higher in IL-4 wild type mice, while IgM and IgG3 anti-DNA levels were significantly higher in IL-4 knockout mice.

A peptide DNA surrogate accelerates autoimmune manifestations and nephritis in lupus-prone mice.

Lupus-associated anti-DNA Abs display features of Ag selection, yet the triggering Ag in the disease is unknown. We previously demonstrated that the peptide DWEYSVWLSN is bound by a pathogenic anti-DNA Ab, and that immunization of nonautoimmune mice with this peptide induces autoantibodies and renal Ig deposition. To elucidate differences in the induced B cell responses in mice genetically predisposed to autoimmunity, young (NZB x NZW)F(1) mice were immunized with this peptide DNA mimetope.

Alpha-actinin is a cross-reactive renal target for pathogenic anti-DNA antibodies.

Anti-DNA Abs commonly found in patients with systemic lupus erythematosus are thought to play an important pathogenic role in lupus nephritis. Anti-DNA Abs may contribute to renal disease by cross-reactivity with renal Ags, the identity of which remain elusive. To identify a target Ag for pathogenic anti-DNA Abs, we performed Western blotting and immunoprecipitations of mesangial cell lysates from the lupus-prone MRL-lpr/lpr mouse and a nonautoimmune BALB/c mouse with the pathogenic anti-DNA Ab R4A.