ライフサイエンスコーパス: SIV

1 SIV evolutionary and selection patterns in non-CD8(+) ly

2 SIV infections of most African primate species also sati

3 SIV skewed macrophages toward resolving phenotypes and e

4 SIV-associated B cell dysfunction associated with the pa

5 SIV-infected CD8-depleted macaques treated with natalizu

6 SIV-infected cells expressed the transcriptional regulat

7 SIV-infected monkeys were treated with a 90-day course o

8 SIV-infected nonhuman primate models are widely used to

9 SIV-infected T cells were numerous within the white pulp

10 in human and primate heart tissue from HIV-1/SIV-infected cells we employed cell and molecular biolog

11 A retrospective neuropathologic review of 30 SIV-infected pigtailed macaques receiving combination an

12 Most dramatically, in acute SIV infection, the expression of almost all target genes

13 Early after SIV infection, the monocyte turnover further increased,

14 imary cells or during the early events after SIV infection and suggest that the level of expression o

15 l immunofluorescence with antibodies against SIV-Gag-p28 and Ki-67, showed that the population of Ki-

16 enteropathogens and that protection against SIV infection by vaccination prevents enteropathogen eme

17 durable protective immune responses against SIV in nonhuman primates.

18 nt and protective antibody responses against SIV in RMs with implications for the design of vaccines

19 Thus, it is possible that AGM SIV populations in milk have unique phenotypic features

20 Although SIV infection resulted in NK cell dysfunction, double-ne

21 d the ability of antibodies induced by ALVAC-SIV/gp120 vaccination, given with alum or MF59 adjuvant,

22 on with the Type I interferon response in an SIV model.

23 nfected CD4(+) T cells and macrophages in an SIV-infected macaque model.

24 -specific CD8(+) T cells in situ by using an SIV-infected rhesus macaque model of HIV.

25 rophage contribution to aspects of HIV-1 and SIV pathogenesis, and their role in viral persistence in

26 Moreover, the HIV-1 and SIV Vif proteins are conserved in terms of their interac

27 Multiple Vpr variants, from HIV-1 and SIV, down-regulate both MUS81 and EME1.

28 ecific differences in layer 3 from HIV-1 and SIV.

29 HIV-1, HIV-2, and SIV Nefs counteract human, ape, monkey, and murine SERIN

30 The interaction between 36D5 and SIV gp120 is similar to the interaction between some bro

31 m protein have decreased the risk of HIV and SIV acquisition.

32 the reasons that primary isolates of HIV and SIV are so heavily resistant to antibody-mediated neutra

33 bility that natural target cells for HIV and SIV in vivo could potentially complete such O-linked car

34 isoforms in natural target cells for HIV and SIV in vivo could result in O-glycosylation of the threo

35 MDSC are partially characterized in HIV and SIV infection, questions remain regarding their persiste

36 characterize viral evolution during HIV and SIV infections.

37 gp120 envelope glycoprotein of both HIV and SIV is N-linked carbohydrate.

38 for the natural replication cycle of HIV and SIV.

39 for the natural replication cycle of HIV and SIV.

40 om lymphoid B cell follicles, where HIV- and SIV-producing cells are most highly concentrated, indica

41 eficiency virus type 1 (HIV-1) in humans and SIV in the macaque model; however, few have attempted to

42 ely detected in both HIV-infected humans and SIV-infected Asian macaques, significant viral infection

43 iants in plasma and milk, whereas humans and SIV-infected rhesus monkeys (RMs), Asian-origin nonnatur

44 Finally, ARVs administered to mice and SIV-infected macaques resulted in neuronal damage and BA

45 on, stimulation, tissue microenvironment and SIV infection and suggest that differential expression o

46 rticle, we study the functional profiles and SIV infection status in vivo of CD4(+) T cells, CD8alpha

47 ns and quantified the frequency of total and SIV Env-specific IL-21(+) TFH cells and total germinal c

48 cephalitis (SIVE) compared to uninfected and SIV-infected animals without encephalitis, a trend that

49 ation marker in the brains of uninfected and SIV-infected macaques with or without encephalitis.

50 Ms was strongly associated with lack of anti-SIV Ab.

51 ith anti-simian immunodeficiency virus (anti-SIV) activity into rhesus macaques 3 days following an i

52 Live attenuated vaccines such as SIV with a deleted nef gene have provided the most robus

53 ble decrease in the level of cell-associated SIV DNA in peripheral blood (average changes of 0.9-, 1.

54 ning how these animals have evolved to avoid SIV disease progression.

55 oinfected with pegiviruses, possibly because SIV causes little to no disease in these hosts.

56 lustrated that Mamu-A2*05:01 is able to bind SIV-epitopes known to evoke a strong CD8(+) T cell respo

57 rnover reflected tissue macrophage damage by SIV and was predictive of terminal disease progression t

58 macaques and subsequent macrophage damage by SIV infection may help explain the basis of more rapid d

59 ities, yet they are unable to be infected by SIV.

60 In contrast to PD-1(+) Tfh cells, SIV-enriched CTLA-4(+)PD-1(-) CD4(+) T cells were found

61 D8 T cells that expand in LNs during chronic SIV infection and may play a significant role in the con

62 r, these results suggest that during chronic SIV infection, despite high levels of exhaustion and lik

63 ollicular SIV-producing cells in chronically SIV-infected rhesus macaques.

64 Interestingly, chronically SIV-infected AGMs have anatomically compartmentalized SI

65 ted AGMs have anatomically compartmentalized SIV variants in plasma and milk, whereas humans and SIV-

66 The CXCR5+ SIV-specific CD8 T cells demonstrated enhanced polyfunct

67 Although delayed SIV acquisition did not predict subsequent viral control

68 t not male rhesus macaques exhibited delayed SIV acquisition.

69 tive coreceptors for entry, which may direct SIV toward CD4(+) T cell subsets and anatomical sites th

70 Expanded MDSC during SIV infection, especially during the post-cART inflammat

71 Despite of the B cell dysfunction, SIV-specific antibody (Ab) production was higher in the

72 We previously showed that in early SIV-infected rhesus macaques intestinal dysfunction is i

73 us 5 host range mutant recombinants encoding SIV Env, Rev, Gag, and Nef followed by two i.m. boosts w

74 the two animals receiving T cells expressing SIV-specific T-cell receptors (TCRs) had significantly f

75 cts of CD8 depletion on levels of follicular SIV-producing cells in chronically SIV-infected rhesus m

76 on by Foxp3(+) cells, a subset of follicular SIV-specific CD8(+) T cells are functional and suppress

77 ned the location and phenotype of follicular SIV-specific CD8(+) T cells in situ, the local relations

78 We found that follicular SIV-specific CD8(+) T cells were able to migrate through

79 b (Rh-alpha4beta7) just before and following SIV infection protected rhesus macaques from developing

80 yers 1 to 3 for HIV-1 and layers 1 and 2 for SIV on gp120 transition to the CD4-bound conformation ha

81 l tissues are major primary target cells for SIV/HIV infection, and massive depletion of these cells

82 dies have shown that CCR5 is dispensable for SIV infection of SM in vivo and that blocking of CCR5 do

83 These data suggest a new paradigm for SIV infection of natural host species, whereby a shared

84 an epidemiology distinct from that found for SIVs in other African primate species.IMPORTANCE Stable

85 g, SIV neutralizing antibodies, or sera from SIV-infected macaques.

86 ociated with reduced infection rates of HIV, SIV, and SHIV.

87 ted with protection from infection with HIV, SIV, and SHIV.

88 ted with protection from infection with HIV, SIV, and SHIV.

89 memory subsets in immune homeostasis and HIV/SIV persistence during antiretroviral therapy (ART) is c

90 the particular characteristics of early HIV/SIV infection in mind, raising the possibility that bett

91 for the investigation of early infection HIV/SIV datasets and, more generally, low diversity viral NG

92 ction factors have been shown to inhibit HIV/SIV replication, little is known about their expression

93 in peripheral blood during the course of HIV/SIV disease.

94 contribute to the asymptomatic phase of HIV/SIV infection, and whether macrophages represent a long-

95 innate immunity and also are targets of HIV/SIV infection.

96 int to their role in the pathogenesis of HIV/SIV infections and suggest that monitoring B cells may b

97 ce for evaluating protective efficacy of HIV/SIV vaccine candidates and that TFH cells play a pivotal

98 ration, quantifying vaccine induction of HIV/SIV-specific TFH cells would greatly benefit vaccine dev

99 Expression of 45 confirmed and putative HIV/SIV restriction factors was analyzed in CD4(+) T cells f

100 POBEC3 (A3) enzymes in primates restrict HIV/SIV replication to differing degrees by deaminating cyto

101 ssion.IMPORTANCE We report here that the HIV/SIV-associated B cell dysfunction (defined by loss of to

102 crophages as an important contributor to HIV/SIV infection in spleen and in promoting morphologic cha

103 human or simian immunodeficiency virus (HIV/SIV) sequences within the brain (compartmentalization) d

104 out altering neutralization by human CD4-Ig, SIV neutralizing antibodies, or sera from SIV-infected m

105 summary, our results suggest that layer 3 in SIV has a greater impact on CD4 binding than in HIV-1.

106 the onset of disease progression to AIDS in SIV-infected adult macaques.

107 in the context of the Mamu-B*008 allotype in SIV-infected rhesus macaques.

108 RT induces specific immunological changes in SIV-infected SMs, thus suggesting that virus replication

109 ge subsets and elicits marked differences in SIV infection and clinical outcomes.

110 est that ANXA1 signaling is dysfunctional in SIV infection, and may contribute to chronic inflammatio

111 d not observe a similar protective effect in SIV-infected African monkeys coinfected with pegiviruses

112 ich Rh-alpha4beta7 may mediate its effect in SIV-infected macaques with implications for understandin

113 rs with regulatory T cells, were enriched in SIV DNA in blood, lymph nodes (LN), spleen, and gut, and

114 y and loss of intraepidermal nerve fibers in SIV-infected macaques.

115 We monitored MDSC frequency and function in SIV-infected rhesus macaques.

116 ), and IL-13 trended significantly higher in SIV-infected AGM milk than in that of RMs, while IL-18 a

117 -18 and IL-6 trended significantly higher in SIV-infected RM milk than in that of AGMs.

118 s are associated with a severe impairment in SIV-specific antibody production.

119 istory of changes in the fecal metagenome in SIV-infected monkeys.

120 We also assessed the cytokine milieu in SIV-infected AGM milk and compared it to that of SIV-inf

121 ses of these macaques with those observed in SIV-noncontrolling and uninfected macaques, we aimed to

122 Here, we have shown that in SIV-infected RMs treated with short-term (i.e., 8-32 wee

123 likely attributable to enhanced turnover in SIV-infected RMs.

124 ing, decreased CD3(+) T cells, and increased SIV-infected cells.

125 Indeed, SIV-specific, Mamu-E-restricted CD8(+) T cells from RM r

126 cinated at birth can develop vaccine-induced SIV-specific IgA and IgG antibodies and cellular immune

127 in natural SIV host species, such as innate SIV/HIV immune factors in milk, as a means of naturally

128 ned that, by day 7 after penile inoculation, SIV has moved first to the inguinal lymph nodes and repl

129 sus macaques 3 days following an intrarectal SIV inoculation.

130 e responses in lymphoid follicles that limit SIV replication in this particular anatomical niche.

131 aged Vpx proteins from a second SIV lineage, SIV of red-capped mangabeys or mandrills (SIVrcm/mnd-2),

132 II molecules have been observed in a macaque SIV vaccine model.

133 lite control in human HIV type 1 and macaque SIV infections, respectively.

134 g cross-species recognition of human and MCM SIV-infected CD4(+) T cells.

135 f followed by two i.m. boosts with monomeric SIV gp120 or oligomeric SIV gp140 proteins.

136 ame cells, the Vpx protein of HIV-2 and most SIVs counteracts SAMHD1.

137 specific TFH cells with systemic and mucosal SIV-specific B cell responses indicate that this cell po

138 e strategies to enhance systemic and mucosal SIV/HIV antibody responses.

139 us can rapidly disseminate following mucosal SIV infection of rhesus monkeys and trigger components o

140 al importance of nonviral factors in natural SIV host species, such as innate SIV/HIV immune factors

141 s than the two control animals receiving non-SIV-specific T cells (means of 4.0 versus 7.5 transmitte

142 hesus monkeys (RMs), Asian-origin nonnatural SIV hosts, do not exhibit this compartmentalization.

143 ion between the pathogenic and nonpathogenic SIV infections, we identified a major difference in conf

144 Our data suggest that, in nonpathogenic SIV infection, NK cells migrate into follicles and play

145 nd absent during the course of nonpathogenic SIV infection in natural nonhuman primate hosts.

146 green monkeys (AGMs), sustain nonpathogenic SIV infections and rarely vertically transmit SIV to the

147 However, the relative ability of SIV envelope glycoproteins to bind or utilize these CD4

148 ked increase in the magnitude and breadth of SIV-specific cellular immune responses in virologically

149 ssue-resident NK cells in a unique cohort of SIV-controlling rhesus macaques that maintained low to u

150 ase progression through continual control of SIV subpopulations from various anatomical compartments

151 n animals that exhibited superior control of SIV.

152 The multiple correlations of SIV Env-specific TFH cells with systemic and mucosal SIV

153 Key factors involved in the benign course of SIV infection in SMs are the absence of chronic immune a

154 The epidemiology of SIV infection in hominoids is characterized by low preva

155 lication in determining the main features of SIV infection in SMs, we treated 12 SMs with a potent an

156 the peripheral blood, MLNs, and BAL fluid of SIV-infected RMs.

157 ped methodology to identify discrete foci of SIV (mac239) infection 48 hr after vaginal inoculation.

158 d with the presence of higher frequencies of SIV-specific CD8 T cells in the GC.

159 pletion and reconstitution, the frequency of SIV-infected CD4(+) T cells before depletion positively

160 er of germinal centers, and the frequency of SIV-specific Ab-secreting cells in B cell zones.

161 In the FRT of SIV(+) macaques, Vdelta1 and Vdelta2 showed comparable l

162 lta2 T cell response in blood and the FRT of SIV-infected macaques contribute to control of viremia.

163 n green monkeys (AGMs) are a natural host of SIV that do not develop simian AIDS.

164 Natural hosts of SIV do not progress to AIDS, in stark contrast to pathog

165 Natural hosts of SIV express very low levels of the canonical entry corec

166 ing Ki-67(+) cells, and (iii) high levels of SIV DNA.

167 Since the significantly higher levels of SIV infection in SLOs occurred with a massive accumulati

168 flammation was associated with low levels of SIV RNA in the brain as shown by in situ hybridization,

169 4(+) T cells exhibited the highest levels of SIV RNA, corresponding to the lower restriction factor e

170 Prolonged ART also decreased the levels of SIV- and HIV-DNA(+) cells, but the estimated size of the

171 oth in humans and in the pathogenic model of SIV infection, and this defect is due to hyperactivation

172 SIV RNA in tissue lysates and the number of SIV RNA-positive cells in tissue sections.

173 Although the number of SIV-DNA-positive cells remained unchanged after CD8 depl

174 cytes and macrophages in the pathogenesis of SIV/HIV and begin to explain why infants are more prone

175 upport to the hypothesis that the paucity of SIV infections in wild populations is a general feature

176 SIVgsn, respectively, also have low rates of SIV infections in their populations.

177 els where macrophage-mediated replication of SIV is thought to occur, how the virus can interact with

178 conformation has been reported, the role of SIV layer 3 remains unknown.

179 macaques during early and chronic stages of SIV infection and compared with SIV-negative controls.

180 inal challenge with a heterologous strain of SIV in animals with TRIM5a restrictive alleles.

181 Many strains of SIV from sooty mangabey monkeys are susceptible to resis

182 TANCE Glycoprotein spikes on the surfaces of SIV and HIV are the sole targets available to the immune

183 age CCR6+ CD4+ T cells as primary targets of SIV during vaginal transmission.

184 infected AGM milk and compared it to that of SIV-infected RMs.

185 oosts with monomeric SIV gp120 or oligomeric SIV gp140 proteins.

186 man or simian immunodeficiency virus (HIV or SIV), respectively, express higher viral loads and progr

187 rentiation, stimulation, tissue location, or SIV infection are currently poorly understood.

188 l proliferation in response to polyclonal or SIV-specific stimulation.

189 Env-specific IgG in protection against oral SIV transmission and control of viral replication in inf

190 CD4-Ig neutralization of SIVmac239 and other SIV isolates.

191 fection levels during the chronic pathogenic SIV infection, restoration is mainly due to an expansion

192 disrupted but not depleted during pathogenic SIV infection.

193 nd in lymph nodes (LNs) following pathogenic SIV infection in a cohort of vaccinated macaques.

194 ignificant role in the control of pathogenic SIV infection.

195 l dysfunction associated with the pathogenic SIV infection is characterized by loss of naive B cells,

196 specifically associated with the pathogenic SIV infection, while in the natural hosts, in which SIV

197 ) is specifically associated with pathogenic SIV infection and absent during the course of nonpathoge

198 es could help prevent infection after penile SIV challenge.

199 acaques at 1, 3, 7, and 14 days after penile SIV inoculation and quantified the levels of unspliced S

200 Post-SIV infection, MDSC were elevated in acute infection and

201 uction of mucosal IgA responses at potential SIV entry sites are associated with better control of vi

202 We used a rapidly progressing SIV/pigtailed macaque model of HIV to examine enteropath

203 fered between nonprogressive and progressive SIV infection models.

204 was morphologically distinct from prototypic SIV encephalitis and human immunodeficiency virus enceph

205 Thus, we quantified SIV and HIV tissue burdens in tissues of infected nonhum

206 In this study, we quantified SIV Env-specific IL-21-producing TFH cells for the first

207 f viral replication, thereby likely reducing SIV morbidity.

208 t virion-packaged Vpx proteins from a second SIV lineage, SIV of red-capped mangabeys or mandrills (S

209 ously reported that the TRIM5alpha-sensitive SIV from sooty mangabeys (SIVsm) clone SIVsmE543-3 acqui

210 Here we show that several SIV isolates, including SIVmac239, are more efficiently

211 f the B cell dysfunction observed in simian (SIV) and human immunodeficiency virus (HIV) infections.

212 acaques with NP adjuvants mixed with soluble SIV Env or a virus-like particle form of Env (VLP) induc

213 the levels of unspliced SIV RNA and spliced SIV RNA in tissue lysates and the number of SIV RNA-posi

214 By 14 days p.i., spliced SIV RNA levels were high in all tissues, but they were t

215 mmune responses in virologically suppressed, SIV-infected monkeys.

216 coreceptors to mediate infection may target SIV toward distinct cell populations that are able to su

217 t restoring CD4(+) TSCM homeostasis and that SIV DNA harbored within this subset contracts more slowl

218 ls are primary targets of infection and that SIV rapidly reaches the regional lymph nodes.

219 Collectively, these data indicate that SIV-associated accumulation of microbial products in the

220 Phenotyping infected cells reveals that SIV has a significant bias for infection of CCR6+ CD4+ T

221 low frequency of CD4(+) cells expressing the SIV coreceptor CCR5.

222 mical locations is readily accessible in the SIV-infected macaque models of neuro-AIDS.

223 nal challenge with wild-type (WT) SIV in the SIV-rhesus macaque model of HIV-1 transmission to women.

224 e a previously unrecognized component of the SIV and HIV reservoir that should be therapeutically tar

225 noclonal antibody (MAb) 36D5 to gp120 of the SIV Env trimer.

226 ral therapy (ART), LTs contained >98% of the SIV RNA(+) and DNA(+) cells.

227 These data suggest that the SIV-associated gastrointestinal disease is associated wi

228 ficantly increased their contribution to the SIV reservoir with prolonged ART-mediated viral suppress

229 signal reflects taxon-specific adaptation to SIV.

230 e exquisite susceptibility of these cells to SIV infection.

231 erential susceptibility of CD4(+) T cells to SIV infection.

232 Low MDSC frequency was observed prior to SIV infection.

233 e, we studied the host responses relevant to SIV targeting of CXCR3(+) CCR5(+) CD4(+) T cells in SLOs

234 response may, in part, confer resilience to SIV-induced intestinal damage.

235 ers of magnitude higher in susceptibility to SIV infection.

236 IV infections and rarely vertically transmit SIV to their infants.

237 n this study, for the first time, we treated SIV-infected sooty mangabeys, a natural host for the inf

238 Here, using ART-treated, SIV-infected rhesus macaques, we show that CTLA-4(+)PD-1

239 utcomes of CNS inflammation in cART-treated, SIV-infected macaques will advance our understanding of

240 As the first non-CD4-tropic SIV, iMac239-DeltaD385 will afford the opportunity to di

241 t was used to derive an infectious R5-tropic SIV lacking a CD4 binding site.

242 ation and quantified the levels of unspliced SIV RNA and spliced SIV RNA in tissue lysates and the nu

243 fter infection) were compared with untreated SIV-infected animals sacrificed at similar times.

244 Using SIV virions whose spikes were "decorated" with the prima

245 m developing AIDS and partially from vaginal SIV acquisition.

246 exception of simian immunodeficiency virus (SIV) (family Retroviridae), the blood-borne viruses harb

247 re infectious simian immunodeficiency virus (SIV) and explored the relationship between virus capture

248 infected with simian immunodeficiency virus (SIV) carrying HIV-1 reverse transcriptase (RT-SHIV), com

249 heterologous simian immunodeficiency virus (SIV) challenge.

250 ype 1 (HIV-1)/simian immunodeficiency virus (SIV) envelope spike (Env) mediates viral entry into host

251 ion following simian immunodeficiency virus (SIV) exposure correlated with rectal plasma cell frequen

252 rus (HIV) and simian immunodeficiency virus (SIV) express a small protein, Nef, to enhance viral path

253 nfection with simian immunodeficiency virus (SIV) has served as an important model of human HIV-1 inf

254 rus (HIV) and simian immunodeficiency virus (SIV) have been described that can utilize the coreceptor

255 igin, natural simian immunodeficiency virus (SIV) hosts, such as African green monkeys (AGMs), sustai

256 experimental simian immunodeficiency virus (SIV) infection in vervet monkeys but not in rhesus macaq

257 IDS caused by simian immunodeficiency virus (SIV) infection is associated with gastrointestinal disea

258 onprogressive simian immunodeficiency virus (SIV) infection models in both natural and nonnatural hos

259 hing systemic simian immunodeficiency virus (SIV) infection, we necropsied male rhesus macaques at 1,

260 on during the simian immunodeficiency virus (SIV) infection.

261 tly available simian immunodeficiency virus (SIV) infectious molecular clones (IMCs) and isolates use

262 ilar, while a simian immunodeficiency virus (SIV) isolate showed significant differences.

263 y virus (HIV)/simian immunodeficiency virus (SIV) lentiviruses.

264 infected with simian immunodeficiency virus (SIV) provide an increasingly utilized model of pathogene

265 rus (HIV) and simian immunodeficiency virus (SIV) replication in human cells is restricted at early p

266 and its HIV-2/simian immunodeficiency virus (SIV) SIVsm paralogue Vpx, hijack the CRL4(DCAF1) E3 ubiq

267 HIV and simian immunodeficiency virus (SIV) target CD4(+) T cells.

268 ural hosts of simian immunodeficiency virus (SIV) that do not progress to AIDS when infected with the

269 h the macaque simian immunodeficiency virus (SIV) vaginal challenge model, we developed methodology t

270 rus (HIV) and simian immunodeficiency virus (SIV) was investigated for its contributions to envelope

271 exposures to simian immunodeficiency virus (SIV), an understanding of processes that promote success

272 iruses HIV-1, simian immunodeficiency virus (SIV), and BIV all form ubiquitin ligase complexes to tar

273 1, as well as simian immunodeficiency virus (SIV), murine leukemia virus (MLV), and the retrotranspos

274 with Mtb and simian immunodeficiency virus (SIV), recapitulating human coinfection.

275 ortas from 16 simian immunodeficiency virus (SIV)- or simian-human immunodeficiency virus (SHIV)-infe

276 tissues from Simian Immunodeficiency Virus (SIV)-infected and uninfected rhesus macaques.

277 ed 20-fold in simian immunodeficiency virus (SIV)-infected animals.

278 dividuals and simian immunodeficiency virus (SIV)-infected Asian macaques, several studies have shown

279 found that in simian immunodeficiency virus (SIV)-infected rhesus macaques (RM), CD4(+) TSCM are pres

280 Simian immunodeficiency virus (SIV)-infected sooty mangabeys (SMs) do not develop AIDS

281 Using the simian immunodeficiency virus (SIV)-macaque model, we tested the immunogenicity and eff

282 population of simian immunodeficiency virus (SIV)-specific CD8 T cells express CXCR5 (C-X-C chemokine

283 us (HIV)- and simian immunodeficiency virus (SIV)-specific CD8(+) T cells are typically largely exclu

284 HIV-1 or any simian immunodeficiency virus (SIV).

285 properties of simian immunodeficiency virus (SIV).

286 unity against simian immunodeficiency virus (SIV).

287 mate hosts of simian immunodeficiency virus (SIV).

288 uses (HIV and simian immunodeficiency virus [SIV]) are of intense interest given the renewed effort t

289 Simian immunodeficiency viruses (SIVs) use their Nef proteins to counteract the restricti

290 ection, while in the natural hosts, in which SIV is nonpathogenic, B cells rapidly increase in both l

291 ic stages of SIV infection and compared with SIV-negative controls.

292 This outcome was correlated with SIV Env-specific rectal IgA, rectal memory B cells, and

293 rformed to address why infants infected with SIV progress more quickly to AIDS than do adults.

294 Rather, they became infected with SIV through cross-species transfer from sooty mangabeys

295 Furthermore, once infected with SIV, infants displayed further increased monocyte turnov

296 ontrast, during nonpathogenic infection with SIV from African green monkeys (SIVagm), follicles remai

297 crease in CD68+Ki-67+ cells in macaques with SIV encephalitis (SIVE) compared to uninfected and SIV-i

298 quence compartmentalization in macaques with SIV-associated CNS neuropathology likely results from la

299 Comparison of this model with SIV-infected non-CD8(+) lymphocyte-depleted macaques als

300 equent vaginal challenge with wild-type (WT) SIV in the SIV-rhesus macaque model of HIV-1 transmissio