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1 er SIVrcm Nef can antagonize tetherin of its natural host.
2 virulence for this Mycoplasma species in its natural host.
3 ew functions involved in colonization of its natural host.
4 erty, which is critical for infection of the natural host.
5 1 is a virulence determinant for ORFV in the natural host.
6 2 is nonessential for virus virulence in the natural host.
7 viruses and their disease potential in their natural host.
8 is not essential for virus virulence in the natural host.
9 volved from low to high conformations in the natural host.
10 r understanding H. pylori persistence in its natural host.
11 of the lethal neurovirulent phenotype in the natural host.
12 n by mouse mammary tumor virus (MMTV) in its natural host.
13 ect important target cell populations of its natural host.
14 me of a pathogenic bacteria recovered from a natural host.
15 es a dicistrovirus that is infectious in its natural host.
16 f such scrapie-associated fragments within a natural host.
17 lent CSFV strain Brescia in infection of the natural host.
18 f PKR in controlling FMDV replication in the natural host.
19 enance of nonpathogenic SIV infection in its natural host.
20 RV) persists predominantly in B cells of its natural host.
21 jejuni employs to achieve commensalism in a natural host.
22 or described, linkingS. suisto pigs as their natural host.
23 ions with a highly pathogenic viruses in the natural host.
24 nd immunity of this novel hepacivirus in its natural host.
25 esponse that developed during infection of a natural host.
26 ntly less able to cause acute disease in the natural host.
27 iral and host determinants of virulence in a natural host.
28 lly known to cause obvious symptoms in their natural hosts.
29 tible species, but is absent in SIV-infected natural hosts.
30 d bird species, which are believed to act as natural hosts.
31 chronic immune activation observed in these natural hosts.
32 ed to the restriction of SIV pathogenesis in natural hosts.
33 nfection pattern similar to SIV infection in natural hosts.
34 in the immune response against Y. pestis in natural hosts.
35 appear to contribute to viral containment in natural hosts.
36 del to study hepacivirus infections in their natural hosts.
37 ed immunodeficiency syndrome (AIDS) in their natural hosts.
38 on during acute and chronic SIV infection in natural hosts.
39 s precious little known about AAV biology in natural hosts.
40 outcomes in SIV infection of natural vs non-natural hosts.
41 ropic DNA viruses that cause tumors in their natural hosts.
42 e regarding the effects of serial passage in natural hosts.
43 e infection of cell lines derived from their natural hosts.
44 ia of the peripheral nervous system in their natural hosts.
45 host range susceptibility, and virulence in natural hosts.
46 ity of primate lentiviruses to spread within natural hosts.
47 irect the virus to different cell targets in natural hosts.
48 eptor CCR5 on CD4(+) T cells of SM and other natural hosts.
50 of FQ-resistant Campylobacter in chicken (a natural host and a major reservoir for C. jejuni) in the
52 ogical activity of cyhv3Il10 on cells of its natural host and indicates that cyhv3Il10 is a true vira
53 ChHV5 replication in cells derived from its natural host and may be crucial not only to better under
54 tial invertebrate hosts, including one known natural host and other potential hosts collected from th
55 s virus (MHV), causes acute hepatitis in its natural host and provides a useful model for understandi
57 eded to study gonococcal pathogenesis in the natural host and to classify strains from direct clinica
58 were developed to study sheep scrapie in the natural host and to investigate potential cofactors in t
60 onses against pathogenic poxviruses in their natural hosts and provide further support for the use of
62 y symbiotic relationship between HBV and its natural host, and highlight the plasticity of the fetal
63 and EV are important for OPV pathogenesis in natural hosts, and whether a system based on F13L orthol
64 specifically induced during infection of the natural host animal by using an in vivo expression techn
66 ned studying FHA using B. bronchiseptica and natural-host animal models should apply to B. pertussis
70 patterns of humoral immune responses in the natural host are therefore more similar to those observe
72 ere we show that (i) acute SIV infections of natural hosts are associated with a rapid and robust typ
74 rogram during pathogenesis compared with the natural host barley despite ~200 million years of reprod
75 ntrol of viral replication and spread in the natural host, but the specific contributions of MDA5 sig
77 STAT1 are required to sustain virulence in a natural host by controlling the inflammatory response ag
78 an immunodeficiency virus (SIV) infection in natural hosts by inoculating Caribbean AGMs with their s
79 ruses tend to cause limited disease in their natural hosts, CAdV A is unusual in that it may cause hi
80 inst an orthopoxvirus (OPV) infection in its natural host can develop in the absence of CD4(+) T cell
82 evidence of an encephalitic DNA virus in its natural host causing increased MMP activity in brains.
83 are relevant to pathogenesis were tested in natural host cell cultures, a model of the human airway
86 s with true virus particles assembled in the natural host cell to assess L2's role in the viral infec
88 the high-risk HPV type 31 (HPV31) enters its natural host cell type via caveola-dependent endocytosis
90 re as a negative control) and macrophages (a natural host cell, used here as a positive control).
94 ches to identify human dermal fibroblasts as natural host cells that support productive MCPyV infecti
96 icantly fewer severe tracheal lesions in the natural host compared to virulent M. gallisepticum R(low
97 on within the lymph node germinal centers of natural hosts contributing to sustained immune competenc
98 s of Antimicrobial Peptides (SMAMPs) imitate natural host-defense peptides, a vital component of the
100 w that plasmacytoid dendritic cells (pDC) of natural hosts display reduced CD4 and/or CCR5 expression
101 Unlike AIDS-susceptible rhesus macaques, natural hosts do not progress to AIDS and resolve immune
102 (SIVs) are generally nonpathogenic in their natural hosts, dramatic increases in pathogenicity may o
106 e aggressive leukaemias and lymphomas in non-natural hosts, expresses seven small nuclear uracil-rich
110 CD4(+) TCM cells of sooty mangabeys (SMs), a natural host for SIV in which infection is nonpathogenic
111 nulin (BgGRN)] from the snail B. glabrata, a natural host for the human blood fluke Schistosoma manso
112 , we treated SIV-infected sooty mangabeys, a natural host for the infection, with a potent antiretrov
120 any species of African nonhuman primates are natural hosts for individual strains of simian immunodef
124 mechanisms underlying the AIDS resistance of natural hosts for simian immunodeficiency virus (SIV) re
125 mmunodeficiency virus (HIV)-infected humans, natural hosts for simian immunodeficiency virus (SIV) ve
128 comparative studies between non-natural and natural hosts for SIV, in which SIV infection results in
129 n only if a prion disease is engendered in a natural host from an infectious prion produced in vitro.
131 mon characteristics with other synthetic and natural host-guest and molecular recognition processes i
132 ymphomagenesis during chronic infection in a natural host has been limited by the exquisite species s
135 It is known that despite high viral loads, natural hosts have a low frequency of CD4(+) cells expre
138 es cellular damage, and persists in its only natural host (humans) are unique and are not fully under
140 ariants were expressed during infection of a natural host, (ii) the structural variation observed in
141 ssociation of MP-derived tubules and PD in a natural host, improving our fundamental understanding of
142 h the pathogenic SIV infection, while in the natural hosts, in which SIV is nonpathogenic, B cells ra
143 our data suggest a unifying model whereby in natural hosts, in which the CCR5 expression level is low
144 f lentiviral infections of seemingly adapted natural hosts, including mechanisms of host control and
146 evolution of virus and host effectors in the natural host, influenza virus evasion of IFITM3 restrict
148 mmunodeficiency virus (SIV) infection in its natural host is characterized by a lack of increased imm
150 ent for Argentine hemorrhagic fever, and its natural host is the New World rodent Calomys musculinus.
151 infection dynamics at the target tissues of natural hosts is central to understanding the mechanisms
152 an immunodeficiency virus (SIV) infection of natural hosts is characterized by nonpathogenic chronic
153 an immunodeficiency virus (SIV) infection of natural hosts is nonpathogenic despite high levels of vi
154 infection in African nonhuman primate (NHP) natural hosts is usually nonpathogenic, despite high lev
155 H7N9) influenza virus infection of chickens (natural hosts) is asymptomatic and that it generates a h
156 ne cells is important for nonpathogenesis of natural hosts, it is possibly not due to its role as a c
161 lity that CXCR6-directed tropism in CCR5-low natural hosts may alter CD4(+) T cell subset targeting c
162 ed in HIV-infected subjects, suggesting that natural hosts may be more appropriate for modeling the i
163 ic stimulation of pDCs by SIV and HIV in non-natural hosts may drive the unrelenting immune system ac
164 n in contributing to the mechanisms ensuring natural host-microorganism communication is in need of f
167 emphasizes the value of our model as a virus-natural-host model to study ocular herpesvirus infection
168 d, in part due to the lack of adequate virus-natural-host models in which to study the cellular and v
169 hat the RVT protein purified from one of its natural hosts, Neurospora crassa, exists in a multimeric
171 es, and when we infected domestic swine, the natural host of CSFV host, we observed that the virus wa
172 d in some stage of chronic infections in the natural host of horses, or the QS genes may be remnants
177 antiviral response in primary cells from the natural host of PRV but is not necessary in nonnatural-h
180 reen monkeys (AGMs; genus Chlorocebus) are a natural host of simian immunodeficiency virus (SIVAGM).
182 ile serology-based approach to determine the natural host of the only known nonprimate hepacivirus (N
183 simian arteriviruses, identify baboons as a natural host of these viruses, and provide further evide
186 type 1 (HIV-1) infections, but they are not natural hosts of HIV-1 or any simian immunodeficiency vi
190 ty in most nonhuman primate species that are natural hosts of simian immunodeficiency virus (SIV) inf
191 M) and sooty mangabeys (SM) are well-studied natural hosts of simian immunodeficiency virus (SIV) tha
196 e course is observed during the infection of natural hosts of SIV infection, such as sooty mangabeys
198 rties of milk of SIV-infected and uninfected natural hosts of SIV, African green monkeys (AGMs), to t
203 monkeys share immunophenotypic features with natural hosts of SIV; that is, low levels of CD4+ T cell
204 t the ADO pathway may be involved in sparing natural hosts of SIVs from developing SIV-related gut dy
205 t preventing cross-species transmission from natural hosts of SIVs to humans in areas of endemicity.
209 ruses in foreign and sometimes even in their natural hosts often stems from the action of potent host
210 ong-lasting bacteremia in reservoir-adapted (natural host or passive carrier of a microorganism) and
211 e transfer and usage of amino acids from the natural host organism Acanthamoeba castellanii to Legion
212 acilitates investigation of noroviruses in a natural host organism and the identification of viral an
217 romelia virus {ECTV}]) despite the lack of a natural host-pathogen relationship with either of these
219 nce in the mouse model; however, its role in natural hosts-pigs, humans, or birds-remains largely unk
221 ance: An understanding of viral evolution in natural host populations is a fundamental goal of virolo
225 MAV-1 produces viral encephalitis in its natural host, providing a good model for studying factor
230 (SIVs), are virtually nonpathogenic in their natural hosts remains a fundamental mystery of modern me
233 genetics to search for mechanisms underlying natural host resistance to infection and identified trig
234 varied routes of transmission from its major natural hosts, ruminant farm animals; and other aspects
237 hich ocular herpes can be studied in a virus-natural-host setting and (ii) it reduces the number of e
239 despite being generally nonpathogenic in its natural host, SIV infection selects for Vif-resistant fo
240 ph nodes during primary SIV infection of the natural host sooty mangabey and the non-natural host pig
242 es characterized by progression to AIDS, and natural host sooty mangabeys (SMs), a species which rema
245 ime suggests that LBV is well adapted to its natural host species and that populations of reservoir h
246 ent of SIV-infected African green monkeys, a natural host species for SIV that does not manifest GI t
247 ic SIV infection of sooty mangabeys (SMs), a natural host species for SIV, is also associated with an
248 bsence of SIV-induced disease progression in natural host species may be partially explained by prese
251 rus (SIV), for which it is the most abundant natural host species, and of a wide range of health-rela
253 SIV infection of sooty mangabeys (SMs), a natural host species, does not cause AIDS despite high-l
255 IDS in SIV-infected sooty mangabeys (SMs), a natural host species, we performed a detailed analysis o
256 suggest a new paradigm for SIV infection of natural host species, whereby a shared outcome of virus-
257 ay be a common feature of SIV replication in natural host species, with the potential to contribute t
260 an immunodeficiency virus (SIV) infection of natural-host species, such as sooty mangabeys (SMs), is
261 n maintaining nonpathogenic SIV infection in natural hosts such as sooty mangabeys (SM) remains to be
264 mmunodeficiency virus (SIV) infection in its natural hosts, such as African green monkeys (AGM) and s
266 livestock, which is applicable to a range of natural host systems, including strains of bovine spongi
267 on SM CD4(+) subsets may delineate distinct natural host target cell populations capable of supporti
270 tive parasite biological states occur in the natural host that are not observed with in vitro cultiva
271 erfect example of virus dissemination by its natural host that may have dramatic public health conseq
272 ition, we summarize the lessons learned from natural hosts that know how to 'show AIDS the door', and
273 of the coevolution between the virus and its natural hosts that led to a nonpathogenic infection.
274 he nonprogressive nature of SIV infection in natural hosts that underlie maintained high levels of pl
278 hese features with those observed in another natural host, the mandrill (MND), we conducted a cross-s
280 quite different from that in the original or natural host, the pathogen may not be suspected based on
282 ission and serial passage of SIVsab from its natural host, the sabaeus African green monkey (AGM), to
283 oup II introns are active in bacteria, their natural hosts, they function inefficiently in eukaryotes
284 pact on the major immune cell populations in natural hosts, thus confirming the nonpathogenic nature
285 lls and limit infection of critical cells in natural hosts, thus contributing to benign outcome of in
286 ould be evaluated using clinical isolates in natural host tissue rather than lab strains of virus in
287 lection when MERS-CoV transmitted from their natural host to human; 3) Six out of nine positive selec
290 phenotypes during long-term colonization of natural hosts to resemble those of their hosts, providin
291 DC3000, was reported to infect not only its natural host tomato but also Arabidopsis in the laborato
292 etic variability of virus replication in the natural host under experimental conditions and no geneti
295 estigate early control of SIV replication in natural hosts, we performed a detailed characterization
296 portance of these findings translated to the natural host, where the AddAB system was found to be req
297 cient evolutionary history of their putative natural hosts, which began diversifying tens of millions
299 gate perturbations in lymphocyte dynamics in natural hosts with nonpathogenic simian immunodeficiency
300 hether coevolution between viruses and their natural host would result in the evasion of IFITM restri
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