A propósito de un caso de rabia humana tratado en Brasil

En el presente trabajo se detallan las características de un caso de rabia en un ser humano.Academia Nacional de Agronomía y Veterinari

A propósito de un caso de rabia humana tratado en Brasil

En el presente trabajo se detallan las características de un caso de rabia en un ser humano.Academia Nacional de Agronomía y Veterinari

Nuevas experiencias sobre la trasmisión de la fiebre aftosa

Los autores han realizado, en una experiencia, un nuevo control de aislamiento al criar, sin que enfermaran de aftosa, cuatro terneros desde su nacimiento y hasta los 18 meses de edad, en un laboratorio donde se manipulean en amplia escala esos virus para producción de vacuna y sueros, y experimentación. Ello confirma que los virus aftosos son de difusibilidad controlable con medidas de aislamiento.Academia Nacional de Agronomía y Veterinari

Nuevas experiencias sobre la trasmisión de la fiebre aftosa

Los autores han realizado, en una experiencia, un nuevo control de aislamiento al criar, sin que enfermaran de aftosa, cuatro terneros desde su nacimiento y hasta los 18 meses de edad, en un laboratorio donde se manipulean en amplia escala esos virus para producción de vacuna y sueros, y experimentación. Ello confirma que los virus aftosos son de difusibilidad controlable con medidas de aislamiento.Academia Nacional de Agronomía y Veterinari

Changes in SARS-CoV-2 viral load and mortality during the initial wave of the pandemic in New York City

Funding: This work was partially supported by the National Center for Advancing Translational Sciences of the National Institutes of Health (UL1 TR0023484 to Julianne Imperato-McGinley) and the National Institute of Allergy and Infectious Diseases (UM1 AI069470 to M.E.S).Public health interventions such as social distancing and mask wearing decrease the incidence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but it is unclear whether they decrease the viral load of infected patients and whether changes in viral load impact mortality from coronavirus disease 2019 (COVID-19). We evaluated 6923 patients with COVID-19 at six New York City hospitals from March 15-May 14, 2020, corresponding with the implementation of public health interventions in March. We assessed changes in cycle threshold (CT) values from reverse transcription-polymerase chain reaction tests and in-hospital mortality and modeled the impact of viral load on mortality. Mean CT values increased between March and May, with the proportion of patients with high viral load decreasing from 47.7% to 7.8%. In-hospital mortality increased from 14.9% in March to 28.4% in early April, and then decreased to 8.7% by May. Patients with high viral loads had increased mortality compared to those with low viral loads (adjusted odds ratio 2.34). If viral load had not declined, an estimated 69 additional deaths would have occurred (5.8% higher mortality). SARS-CoV-2 viral load steadily declined among hospitalized patients in the setting of public health interventions, and this correlated with decreases in mortality.Peer reviewe

Meeting report: 34th international conference on antiviral research

As a result of the multiple gathering and travels restrictions during the SARS-CoV-2 pandemic, the annual meeting of the International Society for Antiviral Research (ISAR), the International Conference on Antiviral Research (ICAR), could not be held in person in 2021. Nonetheless, ISAR successfully organized a remote conference, retaining the most critical aspects of all ICARs, a collegiate gathering of researchers in academia, industry, government and non-governmental institutions working to develop, identify, and evaluate effective antiviral therapy for the benefit of all human beings. This article highlights the 2021 remote meeting, which presented the advances and objectives of antiviral and vaccine discovery, research, and development. The meeting resulted in a dynamic and effective exchange of ideas and information, positively impacting the prompt progress towards new and effective prophylaxis and therapeutics

Lysophosphatidate Induces Chemo-Resistance by Releasing Breast Cancer Cells from Taxol-Induced Mitotic Arrest

Taxol is a microtubule stabilizing agent that arrests cells in mitosis leading to cell death. Taxol is widely used to treat breast cancer, but resistance occurs in 25-69% of patients and it is vital to understand how Taxol resistance develops to improve chemotherapy. The effects of chemotherapeutic agents are overcome by survival signals that cancer cells receive. We focused our studies on autotaxin, which is a secreted protein that increases tumor growth, aggressiveness, angiogenesis and metastasis. We discovered that autotaxin strongly antagonizes the Taxol-induced killing of breast cancer and melanoma cells by converting the abundant extra-cellular lipid, lysophosphatidylcholine, into lysophosphatidate. This lipid stimulates specific G-protein coupled receptors that activate survival signals.In this study we determined the basis of these antagonistic actions of lysophosphatidate towards Taxol-induced G2/M arrest and cell death using cultured breast cancer cells. Lysophosphatidate does not antagonize Taxol action in MCF-7 cells by increasing Taxol metabolism or its expulsion through multi-drug resistance transporters. Lysophosphatidate does not lower the percentage of cells accumulating in G2/M by decreasing exit from S-phase or selective stimulation of cell death in G2/M. Instead, LPA had an unexpected and remarkable action in enabling MCF-7 and MDA-MB-468 cells, which had been arrested in G2/M by Taxol, to normalize spindle structure and divide, thus avoiding cell death. This action involves displacement of Taxol from the tubulin polymer fraction, which based on inhibitor studies, depends on activation of LPA receptors and phosphatidylinositol 3-kinase.This work demonstrates a previously unknown consequence of lysophosphatidate action that explains why autotaxin and lysophosphatidate protect against Taxol-induced cell death and promote resistance to the action of this important therapeutic agent

Virology under the microscope—a call for rational discourse

Viruses have brought humanity many challenges: respiratory infection, cancer, neurological impairment and immunosuppression to name a few. Virology research over the last 60+ years has responded to reduce this disease burden with vaccines and antivirals. Despite this long history, the COVID-19 pandemic has brought unprecedented attention to the field of virology. Some of this attention is focused on concern about the safe conduct of research with human pathogens. A small but vocal group of individuals has seized upon these concerns – conflating legitimate questions about safely conducting virus-related research with uncertainties over the origins of SARS-CoV-2. The result has fueled public confusion and, in many instances, ill-informed condemnation of virology. With this article, we seek to promote a return to rational discourse. We explain the use of gain-of-function approaches in science, discuss the possible origins of SARS-CoV-2 and outline current regulatory structures that provide oversight for virological research in the United States. By offering our expertise, we – a broad group of working virologists – seek to aid policy makers in navigating these controversial issues. Balanced, evidence-based discourse is essential to addressing public concern while maintaining and expanding much-needed research in virology

Timing Is Everything

N. Drayman et al. in their recent article (mBio 8:e01612-17, 2017, https://doi.org/10.1128/mBio.01612-17) have used dynamic proteomics and machine learning to show that the cell cycle state of any individual cell affects the outcome of a productive herpes simplex virus 1 (HSV-1) infection. Cells infected from early G1 through S were most permissive for expression of genes from the HSV-1 genome, whereas cells infected in late G2 to mitosis were much less so. Most of the infected cells that underwent mitosis became permanently nonpermissive for HSV-1 gene expression afterward. The cell cycle stage accounted for 60% of the success of infection, and cell density and motility accounted for most of the rest. To successfully reactivate, HSV-1 must express its genes in neurons and cells of the spinosum and granulosum epidermis strata. These cells are permanently in the cell cycle stages most permissive for HSV-1 gene expression, and none reenters mitosis, thus maximizing the efficiency of a successful HSV-1 reactivation before the adaptive immunity can control it