コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 Viral infection can cause organ dysfunction, but its rol
2 Viral infection can change the expression patterns of di
3 Viral infection is now recognized as a ubiquitous top-do
4 Viral infection is one environmental factor that may con
5 Viral infection underlies a significant share of the glo
6 Viral infections during pregnancy can have devastating c
7 Viral infections trigger host innate immune responses, c
8 Virus infection of cells lacking DUSP11 results in a hig
10 o exert different functions in vivo during a viral infection, in a manner tightly orchestrated in tim
14 birth increases the severity of influenza A virus infections in adult mice by reducing the number of
16 pulations provide averaged information about viral infections, single-cell analyses offer individual
18 ing antibody response is typical of an acute viral infection, with declining neutralizing antibody ti
19 ad T cell activation characteristic of acute viral infection and plasmablast responses reaching >30%
21 d immunity after coronavirus and other acute viral infections, we posit that, with few exceptions, th
22 of tissue-specific effects of primary acute viral infections like COVID-19 are essential for underst
23 biome differences after chronic versus acute viral infections and identify CD8 T cell responses and d
24 es to the prevention of severe disease after virus infection include both a paucity of protective vac
30 both coinfections (1, 2.2%) and alternative viral infections (4, 13.3%) that were not detected by ro
31 y, limiting our understanding of alternative viral infections and coinfections in these patients.
32 NGS to assess the frequencies of alternative viral infections in SARS-CoV-2 RT-PCR-negative PUIs (n =
33 n post-operative inflammation, bacterial and viral infection and infection with or without organ dysf
36 degradation and interferon suppression, and viral infection under interferon-competent conditions.
37 by increased susceptibility to bacterial and viral infections and (to a lesser extent) autoimmune man
41 erge in the development of human cancers and viral infections, but their relevance to bacterial disea
43 the relationships between host genetics and viral infections, the contributions of respiratory viral
46 nge needed to facilitate membrane fusion and virus infection, and the epitope recognized by h5B3.1 ha
49 ty, stimulated by cellular stresses, such as viral infections and ER stress, leads to the regulation
50 , additional environmental triggers, such as viral infections, are usually required to initiate the o
52 , immunizing populations against hepatitis B virus infection, and screening for colorectal cancer.
55 that NF-kappaB is rendered inactive because virus infection results in reduced levels of upstream in
58 provide a possible mechanistic link between viral infection, bloom termination, and mass carbon expo
63 cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, p
65 n, or uncontrolled inflammation triggered by viral infections during pregnancy, and its potential dow
66 IFN-beta are type I IFNs that are induced by virus infection and are important in the host's innate a
67 st innate immunity against hepatitis B and C viral infections by inducing m(6)A modification of viral
69 hroughout her life, leading to a hepatitis C virus infection (which was treated, achieving a sustaine
70 the burden of disease caused by hepatitis C virus infection is proving difficult, despite the availa
71 pproximately 29.6% prevalence of Hepatitis C virus infection observed among inmates studied is high a
74 n associated with an increase in hepatitis C virus infections among women of childbearing age in the
75 chanism by which the pathogenesis of certain viral infections is enhanced in the presence of sub-neut
77 te that chronic lymphocytic choriomeningitis virus infection rapidly triggers severe thymic depletion
78 -I responses to lymphocytic choriomeningitis virus infection were augmented in newly generated mice l
82 g prolonged exposure to Ags, such as chronic viral infections, sustained TCR signaling can result in
86 CE CD8 TCR repertoires responding to chronic viral infections (HIV, hepatitis C virus [HCV], Epstein-
89 he context of the CNS development, acute CNS viral infections, and post-infectious and noninfectious
92 luenza-like illness and laboratory-confirmed viral infection; clinical respiratory illness had incons
105 (d p.i.), although both wild-type and DUBmut virus infections resulted in similar liver pathology.
106 in Nfkbia(NES/NES) mice poorly expand during viral infection, and this can be overcome by exogenous I
112 at other functions pDCs exert in vivo during viral infections is controversial, and more studies are
113 ts into the way that ANP32A might act during virus infection.IMPORTANCE Successful zoonotic transmiss
114 cs and magnitude of the host response during virus infection and demonstrates that inactivating a dom
121 mary receptor for pathogenic NWAs, enhancing viral infection in guinea pigs.IMPORTANCE JUNV is one of
122 tal roles in immune defenses against enteric viral infections by integrating diverse signals, includi
123 of intestinal homeostasis.IMPORTANCE Enteric viral infections are a major cause of gastroenteritis wo
126 sional (3-D) human airway tissues to examine viral infection in a physiologically relevant model syst
127 learned from birth cohort studies examining viral infections and subsequent asthma and from understa
129 ctive in the intestinal epithelium following viral infection, but our understanding of the benefits o
131 al changes were observed and no evidence for viral infection or integration could be provided after l
133 in heavy chain-binding motif were needed for virus infection, whereas the inositol phospholipid-bindi
137 answer outstanding questions regarding giant virus infection mechanisms, we set out to determine biom
139 more than 850 confirmed human cases of H5N1 virus infection have been reported, of which ~60% were f
142 t drugs used to treat human immunodeficiency virus infection, and their use can cause mitochondrial t
143 ry diseases including human immunodeficiency virus infection, psoriasis, rheumatoid arthritis, and sy
144 by acute simian (or human) immunodeficiency virus infection may persist or spontaneously resolve in
146 in response to type I interferons.IMPORTANCE Viral infection triggers the secretion of type I interfe
147 orm of the hepatitis B virus (HBV) genome in viral infection and an undisputed antiviral target for a
151 nds for the potential treatment of influenza viral infections.IMPORTANCE Influenza viruses are highly
154 study, index cases with confirmed influenza virus infection and their household contacts were follow
155 ic and resilient microbiome during influenza virus infection in multiple hosts provides a compelling
156 nsing of the Z-RNA produced during influenza virus infection induces cell death in the form of pyropt
158 on inside an artery resulting from influenza virus infection as the primary outcome of this integrate
164 tudies need to investigate whether influenza virus infection affects susceptibility for aortic dissec
165 ed and antigenically-characterised influenza virus infections from Australia, we investigate the effe
171 A subset of these antibodies can inhibit virus infection, thus making E a suitable candidate for
173 knowledge of the progression of the initial viral infection is limited, and no safe or effective vac
177 attempts to reverse and eliminate the latent viral infection that prevents eradication of the virus.
179 lic reprogramming of host cells during lytic viral infection alters the flow of energy and nutrients
180 to provide quantitative descriptions of many viral infections, but for the Ebola virus, which require
184 tibody levels that may protect against mumps virus infection for longer than previously assumed and i
186 ent signaling pathways in the attenuation of viral infection and may lead to the development of new a
187 ns of the two pathways to the attenuation of viral infection are different in mouse versus human cell
188 and the TLR3 pathways in the attenuation of viral infection may be species specific.IMPORTANCE The m
189 region (MPER) results in robust blocking of viral infection by a class of broadly neutralizing antib
192 pes of RNA sensed by RLRs in the contexts of viral infection, malignancies and autoimmune diseases.
193 gene expression relevant for the control of viral infection, with both proteins potentially facilita
194 ar distinctions drawn between enhancement of viral infection at the plasma membrane and amphipathicit
195 fibrils, known as semen-derived enhancer of viral infection (SEVI), that enhance the viral infectivi
196 ugh recombinant EC1 is a potent inhibitor of viral infection, there is no molecular description of th
197 in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs.
199 Both ARVs and NAbs prevent new rounds of viral infection, but NAbs may have the additional capaci
201 recognition and binding is the first step of viral infection and a key determinant of host specificit
202 organ culture to study the initial steps of viral infection and the consequent innate immune respons
204 ely reflecting their dual role as targets of viral infection and key components of the host response.
206 of environmental exposure on the severity of viral infections, and how the viral genome influences ho
209 ype III IFN for the control and clearance of virus infection, but the physiological basis of this sel
210 ed epitope-tagged proteins in the context of virus infection in order to detect CHPK in the host.
212 -I)-like receptors (RLRs) are key sensors of virus infection, mediating the transcriptional induction
214 ines that contained galbut virus as the only virus infection and showed that these flies can be used
215 lantation monitoring of common opportunistic viral infections and of graft rejection, and should faci
216 nfavorable conditions (e.g. tumor hypoxia or viral infection), canonical, cap-dependent mRNA translat
219 inant Le Blanc delta was able to block Orsay virus infection in worm culture and vice versa, suggesti
220 HIPR-1) as a host factor essential for Orsay virus infection of C. elegans Ablation of HIPR-1 resulte
221 ed for inducing the IPR in response to Orsay virus infection but not in response to other triggers li
222 sting T-cells, SAMHD1 blocks HIV-1 and other viral infections by depletion of the dNTP pool to a leve
227 in humans and is prototypic of a persistent viral infection characterized by periods of latency.
229 immunotherapeutic approaches for persistent viral infections.FUNDINGDeutsche Forschungsgemeinschaft
233 monstrate the differential effect of primary viral infections in the susceptibility to disease exacer
236 f orlistat (tetrahydrolipstatin) in reducing virus infection for several mosquito borne viruses inclu
243 infections, the contributions of respiratory viral infections to patterns of immune development, the
244 universal face masking policy on respiratory viral infections (RVIs) among admitted very-low-birthwei
245 ease is strongly associated with respiratory viral infections, but the impact of viruses on Streptoco
246 is a recognised complication of respiratory virus infections, increasing morbidity and mortality, bu
248 Here, we have shown that upon DNA and RNA viral infection, macrophages reduced 7-dehydrocholestero
249 kably, in response to dsRNA treatment or RNA virus infection, LGP2 is rapidly released from MAVS and
251 rbation in response to a different secondary viral infection and highlight the usefulness of these vi
253 ntial pathogen recognition receptors sensing viral infections while LGP2 has been described as both R
256 terial pigment in controlling herpes simplex virus infection, for which diverse and multimodal antivi
258 t of granule-mediated cytotoxicity, specific viral infections, excess IL-18, and chimeric antigen rec
262 irus (SINV) in Drosophila, here we show that viral infections affect TE transcript amounts via modula
264 ultures with interferon beta-1 abrogated the viral infection, suggesting one potential mechanism for
266 s integral for mechanistic insights into the viral infection cycle, very little is known about the lo
267 We performed serological profiling of the viral infection history in 899 individuals from an NCI-U
271 ylate (cOA) second messengers in response to viral infection of bacteria and archaea, potentiating an
280 SAMHD1 suppresses innate immune responses to viral infection and inflammatory stimuli by inhibiting t
281 late innate and adaptive immune responses to viral infection by engaging with receptors on immune cel
282 eletion increases cellular susceptibility to viral infection in vitro, and that Snx5 knockout in mice
289 .51; 95% CI = 4.37-12.91), respiratory tract viral infection (OR = 7.75; 95% CI = 1.60-37.57), cytome
290 prior or concurrent upper respiratory tract viral infection, this bacterium commonly causes multiple
291 Despite global efforts to prevent and treat virus infections to limit morbidity and mortality, the c
292 in mediating antiviral protection in various viral infections, necessitating a detailed understanding
299 es during epidemics.IMPORTANCE Although Zika virus infection of pregnant women can result in congenit