Diabrotica virgifera virgifera larvae are root-feeding insects and significant pests to maize in North America and Europe. Little is known regarding how plants respond to insect attack of roots, thus complicating the selection for plant defense targets. Diabrotica virgifera virgifera is the most successful species in its genus and is the only Diabrotica beetle harboring an almost species-wide Wolbachia infection. Diabrotica virgifera virgifera are infected with Wolbachia and the typical gut flora found in soil-living, phytophagous insects. Diabrotica virgifera virgifera larvae cannot be reared aseptically and thus, it is not possible to observe the response of maize to effects of insect gut flora or other transient microbes. Because Wolbachia are heritable, it is possible to investigate whether Wolbachia infection affects the regulation of maize defenses. To answer if the success of Diabrotica virgifera virgifera is the result of microbial infection, Diabrotica virgifera virgifera were treated with antibiotics to eliminate Wolbachia and a microarray experiment was performed. Direct comparisons made between the response of maize root tissue to the feeding of antibiotic treated and untreated Diabrotica virgifera virgifera show down-regulation of plant defenses in the untreated insects compared to the antibiotic treated and control treatments. Results were confirmed via QRT-PCR. Biological and behavioral assays indicate that microbes have integrated into Diabrotica virgifera virgifera physiology without inducing negative effects and that antibiotic treatment did not affect the behavior or biology of the insect. The expression data and suggest that the pressure of microbes, which are most likely Wolbachia, mediate the down-regulation of many maize defenses via their insect hosts. This is the first report of a potential link between a microbial symbiont of an insect and a silencing effect in the insect host plant. This is also the first expression profile for a plant attacked by a root-feeding insect.
Chikungunya virus (CHIKV) was first extensively described in children during outbreaks in India and South Asia during the mid-1960s. Prior to the 2005 emergence of CHIKV on Reunion Island, CHIKV infection was usually described as a dengue-like illness with arthralgia in Africa and febrile hemorrhagic disease in Asia. Soon after the 2005 emergence, severe CNS consequences from vertical and perinatal transmission were described and as CHIKV continued to emerge in new areas over the next 10 years, severe manifestation of infection and sequelae were increasingly reported in infants and neonates. The following review describes the global reemergence and the syndromes of Chikungunya fever (CHIKF) in infants and children. The various manifestations of CHIKF are described and connected to the viral lineage that was documented in the area at the time the disease was described. The data show that certain manifestations of CHIKF occur with specific viral lineages and genetic motifs, which suggests that severe manifestations of CHIKF in the very young may be associated with the emergence of new viral lineages.
Like most of the world, Pakistan has seen an increase in mosquito-transmitted diseases in recent years. The magnitude and distribution of these diseases are poorly understood as Pakistan does not have a nation-wide system for reporting disease. A cross-sectional study to determine which flaviviruses were causing of arboviral disease in Pakistan was instituted. West Nile virus (WNV) is a cause of seasonal fever with neurotropic findings in countries that share borders with Pakistan. Here, we describe the active and persistent circulation of WNV in humans in the southern region of Pakistan. This is the first report of WNV causing neurological disease in human patients in this country. Of 997 enrolled patients presenting with clinical features suggestive of arboviral disease, 105 were positive for WNV IgM antibodies, and 71 of these patients possessed WNV-specific neutralizing antibodies. Cross-reactivity of WNV IgM antibodies with Japanese encephalitis virus (JEV) occurred in 75 of these 105 patients. WNV co-infections with Dengue viruses were not a contributing factor for the severity of disease. Nor did prior exposure to dengue virus contribute to incidence of neurological involvement in WNV-infected patients. Patients with WNV infections were more likely to present with altered mental status, seizures, and reduced Glasgow Coma scores when compared with JEV-infected patients. Human WNV cases and vector numbers exhibited a temporal correlation with climate.
Several arboviruses are endemic to and co-circulate in Pakistan. In recent years, Pakistan has observed a rise in arboviral infections. A cross-sectional study for arboviral diseases, which included screening for Chikungunya virus (CHIKV), was initiated in 2015 to determine which pathogens were causing disease in patients presenting to health care services. Exposure to CHIKV was verified via detection of viral nucleic acids or virus-specific IgM with virus-specific neutralizing antibodies. Out of 997 enrolled patients presenting with clinical features suggestive of arboviral disease, 102 patients were positive for CHIKV IgM antibodies and 60 patients were positive for CHIKV nucleic acids or neutralizing antibodies. The data presented here show that CHIKV has been circulating in Pakistan since April of 2015. CHIKV infections were detected in study subjects up to the conclusion of our enrollment period in July 2017. Syndromic and clinical data show that arthralgia was associated with CHIKV as was rash, fever greater than 38°C, and lymphopenia. Neurological symptoms were reported in 49% of CHIKV suspect patients and in 46.6% of confirmed infections. Acute disseminated encephalomyelitis was diagnosed in 5% of confirmed infection and various manifestation of encephalitis diagnosed in an additional 16.6% of patients with confirmed CHIKV infections. CHIKV-exposed patients were just as likely to present with neurological symptoms and encephalitis as patients with West Nile Virus infections but were 4.57 times more likely to have lymphopenia. This proportion of neurological symptoms may be a complicating factor in countries where WNV and/or JEV co-circulate with CHIKV.
Aim: This study investigated the stability of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on 16 common environmental surface materials. Background: SARS-CoV-2 is the causative agent of severe coronavirus disease, a significant public health concern that quickly led to a pandemic. Contamination of environmental surface materials is of concern, with previous studies identifying long-term detection of infectious particles on surfaces. These contaminated surfaces create an increased risk for contact transmission. Methods: Surface materials were inoculated with 10,000 plaque forming units and samples were collected 4, 8, 12, 24, 30, 48, and 168 hours post infection (hpi). Viral titers were determined for each sample and time point using plaque assays. Nonparametric modeling utilized the Turnbull algorithm for interval-censored data. Maximum likelihood estimates for the survival curve were calculated. Parametric proportional hazards regression models for interval censored data were used to explore survival time across the surface materials. Results: There was a sharp decline in recoverable virus after 4 hpi for all tested surfaces. By 12 hpi, infectious SARS-CoV-2 was recoverable from only four surfaces; and by 30 hr, the virus was recoverable from only one surface. There were differences in survival curves based on the materials although some groups of materials are similar, both statistically and practically. Conclusions: While very low amounts of infectious SARS-CoV-2 are recoverable over time, there remains a risk of viral transmission by surface contamination in indoor environments. Individuals and institutions must follow appropriate procedures to decontaminate indoor environment and increase diligence for hand hygiene and personal protective equipment.
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