BackgroundThe United States' COVID-19 epidemic has grown extensively since February 2020, with substantial associated hospitalizations and mortality; New York State (NYS) has emerged as the national epicenter. We report on the extent of testing and test results during the month of March in NYS, along with risk factors, outcomes, and household prevalence among initial cases subject to indepth investigations. MethodsSpecimen collection for COVID-19 testing was conducted in healthcare settings, community-based collection sites, and by home testing teams. Information on demographics, risk factors, and hospital outcomes of cases was obtained through epidemiological investigations and an electronic medical records match, and summarized descriptively. Active testing of initial case's households enabled estimation of household prevalence. ResultsDuring March In NYS, outside of New York City, a total of 47,326 persons tested positive for SARS-CoV-2, out of 141,495 tests (33% test-positive), with the highest number of cases located in the metropolitan region counties. Among 229 initial cases diagnosed through March 12, by March 30 13% were hospitalized and 2% died. Testing conducted among 498 members of these case's households found prevalent infection among 57%; excluding first-reported cases 38%. In these homes, we found a significant age gradient in prevalence, from 23% among those <5 years to 68% among those ≥65 years (p<.0001). ConclusionsNew York State faced a substantial and increasing COVID-19 outbreak during March 2020. The earliest cases had high levels of infection in their households and by the end of the month, the risks of hospitalization and death were high.

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The performance and interpretation of laboratory tests for Zika virus (ZKV) continue to be evaluated. Serology is cross-reactive, laborious, and frequently difficult to interpret, and serum was initially solely recommended for molecular diagnosis. ZKV testing was initiated in January 2016 in New York State for symptomatic patients, pregnant women, their infants, and patients with Guillain-Barré syndrome who had traveled to areas with ZKV transmission. Subsequently, eligibility was expanded to pregnant women with sexual partners with similar travel histories. Serum and urine collected within 4 weeks of symptom onset or within 6 weeks of travel were tested with real-time reverse transcription-PCR (RT-PCR) assays targeting the ZKV envelope and NS2B genes. In this review of lessons learned from the first 80 positive cases in NYS, ZKV RNA was detected in urine only in 50 patients, in serum only in 19 patients, and in both samples concurrently in 11 patients, with average viral loads in urine a log higher than those in serum. Among 93 positive samples from the 80 patients, 41 were positive on both gene assays, 52 were positive on the envelope only, and none were positive on the NS2B only. Of the 80 infected patients, test results for 74 (93%) would have defined their infection status as not detected or equivocal if the requirement for positive results from two assay targets (two-target-positive requirement) in the initial federal guidance to public health laboratories was enforced, if urine was not tested, or if the extended eligibility time for molecular testing was not implemented. These changes facilitated more extensive molecular diagnosis of ZKV, reducing reliance on time-consuming and potentially inconclusive serology.

Group B coxsackieviruses are associated with chronic inflammatory diseases of the pancreas, heart, and central nervous system. Chronic pancreatitis, which can develop from acute pancreatitis, is considered a premalignant disorder because it is a major risk factor for pancreatic cancer. To explore the genetic events underlying the progression of acute to chronic disease, a comparative analysis of global gene expression during coxsackievirus B4-induced acute and chronic pancreatitis was undertaken. A key feature of acute pancreatitis that resolved was tissue regeneration, which was accompanied by increased expression of genes involved in cell growth, inhibition of apoptosis, and embryogenesis and by increased division of acinar cells. Acute pancreatitis that progressed to chronic pancreatitis was characterized by lack of tissue repair, and the expression map highlighted genes involved in apoptosis, acinoductular metaplasia, remodeling of the extracellular matrix, and fibrosis. Furthermore, immune responses appeared skewed toward development of alternatively activated (M2) macrophages and T helper 2 (Th2) cells during disease that resolved and toward classically activated (M1) macrophages and Th1 cells during disease that progressed. Our hypothesis is that growth and differentiation signals coupled with the M2/Th2 milieu favor acinar cell proliferation, while diminished growth signals and the M1/Th1 milieu favor apoptosis of acinar cells and remodeling/proliferation of the extracellular matrix, resulting in fibrosis.The group B coxsackieviruses are associated with chronic inflammatory diseases of the pancreas (insulin-dependent diabetes mellitus and idiopathic chronic pancreatitis), heart (dilated cardiomyopathy), and central nervous system (12). Efforts to elucidate the mechanisms by which these viruses cause disease have focused on identifying the molecular determinants of viral virulence and understanding the immune response to infection. The molecular determinants of viral virulence for the group B coxsackieviruses are distinct, suggesting that these viruses induce disease via diverse mechanisms. For coxsackievirus B3 (CVB3), determinants of attenuation and virulence have been identified in the 5Ј untranslated region (42) and in VP2 (21). For CVB4, Thr-129 of VP1 is a major determinant of virulence (11). The precise mechanism by which the viral molecular determinants cause tissue injury is not clear. During coxsackievirus B infection, both virus-induced cytopathology and immunopathological mechanisms have been implicated in mediating tissue injury (12, 36).Our mouse model uses two serologically indistinguishable variants of the CVB4 serotype that cause acute and chronic pancreatitis reminiscent of clinical disease. The CVB4-P variant induces a transient, acute disease which shares pathological features (edema and inflammation) (34) with acute, interstitial pancreatitis in humans (9). The CVB4-V variant induces a severe, acute disease which progresses to chronic pancreatitis. CVB4-V-induced chronic pancreatitis ...