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Herpes zoster (HZ) vaccine was recommended in the United States to reduce HZ-associated morbidity. Vaccination may reduce HZ-associated mortality, but no strategy exists to monitor mortality trends.We validated HZ coding on death certificates from California, using hospital records as the gold standard, and applied the results to national-level data to estimate HZ mortality.In the validation phase of the study, among 40 available hospital records listing HZ as the underlying cause of death, HZ was the underlying cause for 21 (52.5%) and a contributing cause for 5 (12.5%). Among the 21 hospital records listing HZ as the underlying cause of death, the median age of decedents was 84 years (range, 50-99); 60% had no contraindications for HZ vaccination. Of the 37 available records listing HZ as a contributing cause of death, HZ was a contributing cause for 2 (5.4%) and the underlying cause for 6 (16.2%). Nationally, in the 7 years preceding the HZ vaccination program, the average annual number of deaths in which HZ was reported as the underlying cause of death was 149; however, based on our validation study, we estimate the true number was 78 (range, 31-118).National death certificate data greatly overestimate deaths in which HZ is the underlying or contributing cause of death. The HZ vaccination program could prevent some HZ-related deaths, but the impact will be difficult to assess using national mortality data.

In October and November 2010, hospitals in northern Uganda reported patients with suspected hemorrhagic fevers. Initial tests for Ebola viruses, Marburg virus, Rift Valley fever virus, and Crimean Congo hemorrhagic fever virus were negative. Unbiased PCR amplification of total RNA extracted directly from patient sera and next generation sequencing resulted in detection of yellow fever virus and generation of 98% of the virus genome sequence. This finding demonstrated the utility of next generation sequencing and a metagenomic approach to identify an etiological agent and direct the response to a disease outbreak.

The first confirmed Rift Valley fever outbreak outside Africa was reported in September 2000, in the Arabian Peninsula. As of February 2001, a total of 884 hospitalized patients were identified in Saudi Arabia, with 124 deaths. In Yemen, 1,087 cases were estimated to have occurred, with 121 deaths. Laboratory diagnosis of Rift Valley fever virus (RVFV) infections included virus genetic detection and characterization of clinical specimens by reverse transcription-polymerase chain reaction, in addition to serologic tests and virus isolation. Genetic analysis of selected regions of virus S, M, and L RNA genome segments indicated little genetic variation among the viruses associated with disease. The Saudi Arabia and Yemen viruses were almost identical to those associated with earlier RVF epidemics in East Africa. Analysis of S, M, and L RNA genome segment sequence differences showed similar phylogenetic relationships among these viruses, indicating that genetic reassortment did not play an important role in the emergence of this virus in the Arabian Peninsula. These results are consistent with the recent introduction of RVFV into the Arabian Peninsula from East Africa.

Sin Nombre virus (SNV) is a major representative of the New World hantaviruses and the most common cause of hantavirus pulmonary syndrome (HPS) with high mortality in North America. Unlike other members of the family Bunyaviridae which mature in the Golgi complex, New World hantaviruses have been previously reported to mature at the cell surface. For family Bunyaviridae viruses, retention of the viral glycoproteins at the Golgi complex is thought to be responsible for their Golgi maturation. In our studies, the majority of SNV glycoproteins, G1 and G2, was localized in the Golgi complex when expressed from a full-length GPC clone or in SNV-infected cells, in agreement with data for other members of the family Bunyaviridae, including the Old World hantaviruses. However, the SNV glycoproteins could also be detected at the cell surface at advanced posttransfection or postinfection time points. G1 expressed in the absence of G2 did not accumulate in the Golgi, but remained predominantly associated with the endoplasmic reticulum (ER). Overexpressed amounts of apparently misfolded G1 were aggregated in a subcellular compartment likely to represent the aggresome. Unexpectedly, an additional major pool of G1 was detected intracellularly in SNV-infected and GPC-expressing transfected cells, by using a SNV G1-specific Fab antibody. This pool of G1 is predominantly localized in late endosomes–lysosomes.