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1.
Annu Rev Cell Dev Biol ; 37: 171-197, 2021 10 06.
Artículo en Inglés | MEDLINE | ID: mdl-34270326

RESUMEN

Viral egress and transmission have long been described to take place through single free virus particles. However, viruses can also shed into the environment and transmit as populations clustered inside extracellular vesicles (EVs), a process we had first called vesicle-mediated en bloc transmission. These membrane-cloaked virus clusters can originate from a variety of cellular organelles including autophagosomes, plasma membrane, and multivesicular bodies. Their viral cargo can be multiples of nonenveloped or enveloped virus particles or even naked infectious genomes, but egress is always nonlytic, with the cell remaining intact. Here we put forth the thesis that EV-cloaked viral clusters are a distinct form of infectious unit as compared to free single viruses (nonenveloped or enveloped) or even free virus aggregates. We discuss how efficient and prevalent these infectious EVs are in the context of virus-associated diseases and highlight the importance of their proper detection and disinfection for public health.


Asunto(s)
Vesículas Extracelulares , Virus , Vesículas Extracelulares/metabolismo , Virus/genética
2.
Artículo en Inglés | MEDLINE | ID: mdl-32432225

RESUMEN

With growth and exponential globe trotter traveling of the human population, and many more conducive factors, the likelihood of merging and melting viruses capable of infecting humans in a cooperative fashion, has increased markedly. Hence, viruses that were limited to a particular region of the planet, or to certain population groups, have become capable of infecting humans on a pandemic scale. Some viruses not only can infect pregnant women, but also expand to the amnotic fluid and fetus. With this review, we will reflect upon some examples of known viral cooperations, as well as new ones that have the potential for compromising human health and survival of the fetus in utero.

3.
Antioxid Redox Signal ; 27(9): 511-516, 2017 Sep 20.
Artículo en Inglés | MEDLINE | ID: mdl-28482684

RESUMEN

Alzheimer's drugs are failing at a rate of 99.6%, and success rate for drugs designed to help patients with this form of dementia is 47 times less than for drugs designed to help patients with cancers ( www.scientificamerican.com/article/why-alzheimer-s-drugs-keep-failing/2014 ). How can it be so difficult to produce a valuable drug for Alzheimer's disease? Each human has a unique genetic and epigenetic makeup, thus endowing individuals with a highly unique complement of genes, polymorphisms, mutations, RNAs, proteins, lipids, and complex sugars, resulting in distinct genome, proteome, metabolome, and also microbiome identity. This editorial is taking into account the uniqueness of each individual and surrounding environment, and stresses the point that a more accurate definition of a "common" disorder could be simply the amalgamation of a myriad of "rare" diseases. These rare diseases are being grouped together because they share a rather constant complement of common features and, indeed, generally respond to empirically developed treatments, leading to a positive outcome consistently. We make the case that it is highly unlikely that such treatments, despite their statistical success measured with large cohorts using standardized clinical research, will be effective on all patients until we increase the depth and fidelity of our understanding of the individual "rare" diseases that are grouped together in the "buckets" of common illnesses. Antioxid. Redox Signal. 27, 511-516.


Asunto(s)
Diseño de Fármacos , Predisposición Genética a la Enfermedad , Enfermedad de Alzheimer/tratamiento farmacológico , Humanos , Medicina de Precisión , Enfermedades Raras/tratamiento farmacológico
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