bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epidemic of adenovirus‐induced respiratory illness among US military recruits: Epidemiologic and immunologic risk factors in healthy, young adults*†
Authors: Sanchez Jose L. , Binn Leonard N. , Innis Bruce L. , Reynolds Richard D. , Lee Terrence , Mitchell‐Raymundo Felicia , Craig Stephen C. , Marquez Jeffrey P. , Shepherd Greg A. , Polyak Christina S. , Conolly Johnnie , Kohlhase Kimmie F. 
Published: August 2002

AbstractAdenovirus (Ad)‐induced acute respiratory illnesses resurged among civilian adults and selected military training populations in the United States during the late 1990s. We examined the epidemiologic and immunologic correlates of Ad‐induced respiratory illnesses during a large outbreak at an Army basic training installation in southeast United States during a 9‐day period in November 1997. A total of 79 recruits hospitalized with acute respiratory illnesses were evaluated during the outbreak period; confirmation of Ad infection by isolation of Ad‐like cytopathic agents from throat cultures was detected in 71 (90%) of these patients. Serotyping of 19 (27%) of these 71 isolates identified the etiologic agent to be Ad type 4 (Ad4). In addition, 30 (81%) of 37 patients in whom paired sera were collected demonstrated significant increases (i.e., 4‐fold or higher) in serum anti‐Ad4 neutralizing antibodies. Anti‐Ad4 immunity in new recruits was found to be very low (15 to 22%). A case‐control study involving 66 of the 79 hospitalized cases and 189 non‐ill controls from the same units was conducted. A lower risk of hospitalization for acute respiratory illnesses was documented for female recruits (odds ratio[OR] = 0.47, P < .05) whereas, a higher risk was noted for smokers (OR = 1.89, P < .05). Unit (training company) attack rates as high as 8 to 10% per week were documented and the outbreak quickly subsided after live, oral Ad types 4 and 7 vaccination was resumed in November 1997. Re‐establishment of a military Ad vaccination program is critical for control of Ad‐induced acute respiratory illnesses. J. Med. Virol. 65:710–718, 2001. © 2001 Wiley‐Liss, Inc.
Antibody convergence along a common idiotypic axis in immunodeficiency virus and hepatitis C virus infections
Authors: Grant Michael D. 
Published: August 2002

AbstractThe anti‐idiotypic antibody 1F7 selectively binds antibodies against human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) gag, pol, and env proteins. We tested anti‐hepatitis C virus (HCV) antibodies to investigate selection of the 1F7 idiotype on antibodies against other chronic pathogens. Twelve of 15 HCV‐seropositive individuals co‐infected with HIV had detectable antibodies against recombinant HCV core, 4 against HCV NS4 protein, and 3 against HCV NS3 protein. All four HCV‐seropositive, non‐HIV‐infected individuals had antibodies against HCV core and NS4, while 3 had antibodies against NS3. The 1F7 idiotype was frequently present on antibodies against each of the HCV antigens in the HIV co‐infected and non‐HIV‐infected groups. Antibodies against HCV, including antibodies recognizing the putative principal neutralizing determinant of HCV E2 protein, displayed skewed κ/λ light chain usage consistent with clonal dominance. These observations extend the association between expression of the 1F7 idiotype and abnormal B cell clonal dominance in HIV and SIV infection to HCV infection and suggest that early establishment of an oligoclonal antibody response against HCV may freeze the B cell repertoire, impair adaptation to emergent HCV variants, and favor escape from neutralizing antibodies. We also demonstrated that expression of the 1F7 idiotype extends beyond antibodies against multiple antigens of AIDS‐causing retroviruses to include antibodies against multiple antigens of an unrelated chronic hepatitis virus. Thus, distinct pathogens establishing chronic infection in the face of strong humoral immune responses select antibodies along a common idiotypic axis of the immune network. J. Med. Virol. 66:13–21, 2002. © 2002 Wiley‐Liss, Inc.
Fatal adult case of severe lymphocytopenia associated with reactivation of human herpesvirus 6
Authors: Yoshikawa Tetsushi , Ihira Masaru , Asano Yoshizo , Tomitaka Akiko , Suzuki Kayoko , Matsunaga Kayoko , Kato Yasuchika , Hiramitsu Sinya , Nagai Tomohito , Tanaka Naoko , Kimura Hiroshi , Nishiyama Yukihiro 
Published: August 2002

AbstractIt has been suggested that immunosuppression associated with human herpesvirus 6 (HHV‐6) infection is a result of functional impairment or direct destruction of immunological cells. The ability of the virus to infect and destroy lymphocytes may cause progressive immunodeficiency in an infant with primary HHV‐6 infection. An adult patient is described who had a fatal cytomegalovirus (CMV) infection due to severe and prolonged lymphocyte depletion associated with HHV‐6 reactivation. The HHV‐6 antibody titers were increased significantly after reactivation, and the virus was isolated from his peripheral blood mononuclear cells. The quantity of both HHV‐6 and CMV DNA was determined by using real‐time PCR in plasma samples collected serially. HHV‐6 DNAemia persisted for 1 month, which started just 1 week after the onset of lymphocytopenia. In contrast to HHV‐6, CMV DNAemia was detected in the terminal phase of the illness. Thus, HHV‐6 reactivation may have been the cause of the severe lymphocyte depletion and fatal CMV infection. J. Med. Virol. 66:82–85, 2002. © 2002 Wiley‐Liss, Inc.
Expression of cytokeratin 16 in human papillomavirus type 11‐infected genital epithelium
Authors: McClowry Tracy L. , Shors Teri , Brown Darron R. 
Published: August 2002

AbstractDuring normal keratinocyte differentiation, a coordinated expression of many cytoskeletal and regulatory proteins occurs. Several studies suggest that expression of some of these proteins is altered in epithelium infected by the human papillomavirus (HPV). To examine protein expression, human foreskin tissue was infected with either the low‐risk HPV type 11 or with HPV 83, a high‐risk type. The foreskin tissue was implanted and grown in the athymic mouse xenograft system. Immunohistochemistry and immunoblot analysis of human foreskin xenografts were performed to detect cytokeratin 16 (K16), a protein previously identified in proliferative disorders of the skin. K16 was abundant in HPV 11‐infected xenograft tissue, but was not detected in uninfected or HPV 83‐infected tissue. Analysis of protein extracted from human biopsy tissue demonstrated the same expression patterns in natural infection by HPV 11. Reverse transcriptase PCR detected mRNA transcripts for K16 in both experimental and natural HPV 11‐infected tissues, but not in uninfected tissue. These studies suggest that K16 overexpression during HPV 11‐infection is regulated at the level of transcription. The marked epithelial proliferation that occurs in HPV 11 infection may involve alterations in expression of cytoskeletal proteins, including K16. Determining the mechanisms of K16 transcriptional induction could lead to therapies with the ability to reduce cell proliferation within infected tissue. J. Med. Virol. 66:96–101, 2002. © 2002 Wiley‐Liss, Inc.
Genetic variations of human herpesvirus 7 by analysis of glycoproteins B and H, and R2‐repeat regions
Authors: Thawaranantha Duanthanorm , Chimabutra Kanittha , Balachandra Kruavon , Warachit Paijit , Pantuwatana Somsak , Tanaka‐Taya Keiko , Inagi Reiko , Kurata Takeshi , Yamanishi Koichi 
Published: August 2002

AbstractClinical isolates of human herpesvirus 7 (HHV‐7) from the saliva of healthy individual were investigated for genetic variations in the regions of two immediate‐early (IE) genes, the glycoprotein B (gB) and glycoprotein H (gH) genes, and in R2‐repeat. The genomic DNA of 24 isolates from citizens of Thailand, Japan, and the United States was amplified to detect size variations in the IE‐1 and IE‐2 loci, but none was observed, suggesting that there was no deletion or insertion in these genes, in contrast with an IE gene of human herpesvirus 6 (HHV‐6). The sequences of the gB gene from isolates acquired from 5 Japanese and 8 Thai subject were then compared with those of American strains JI and RK with respect to codons that are known to differentiate gB alleles. All the isolates were found to have gB allele C except for the JI strain, which has allele F. Variability was also observed in five specific gH codons, resulting in 6 different groups. The HHV‐7 isolates might be classified into two major genetic variants by combining their gB and gH allelic groupings. In the present study, only JI belonged to variant 1, while the rest of the isolates appeared to belong to variant 2. In the R2‐repeat region, size heterogeneities were observed among the 24 isolates, due to different repeat numbers (17, 15, 14, 13, or 12 repeats). Therefore, we used the R2‐repeat to identify the origins of isolates in a study of HHV‐7 transmission, and found HHV‐7 to be transmitted within a family from both mothers and fathers to their children. J. Med. Virol. 66:370‐377, 2002. © 2002 Wiley‐Liss, Inc.
Minimal reactivation of Kaposi's sarcoma‐associated herpesvirus by corticosteroids in latently infected B cell lines
Authors: Zoeteweij J. Paul , Rinderknecht Andrea S. , Davis David A. , Yarchoan Robert , Blauvelt Andrew 
Published: August 2002

AbstractCorticosteroid use in transplant recipients increases the incidence and severity of Kaposi's sarcoma (KS), a disease associated with KS‐associated herpesvirus (KSHV) infection. Recently, the prototypic corticosteroid, hydrocortisone, was shown to directly induce lytic cycle reactivation of KSHV in latently‐infected BCBL‐1 cells. The purpose of this study was to examine this phenomenon in further detail. After incubation with dexamethasone (≤ 30 μM) or hydrocortisone (≤ 30 μM) for 1–4 days, we evaluated KSHV reactivation in latently infected B cell lines (BC‐1, BC‐3, and BCBL‐1) by assessing early‐lytic PF‐8 and late‐lytic gpK8.1 protein expression using flow cytometry. Viral particle production was monitored by quantifying KSHV minor capsid protein levels in cell culture supernatants. A small increase in the percentage of cells expressing viral lytic proteins was observed in BCBL‐1, but not in the other cell lines. In combination with 3 nM 12‐O‐tetradecanoyl‐phorbol‐13‐acetate, a known chemical inducer of KSHV replication, corticosteroids (0.3 μM) enhanced KSHV reactivation twofold in some cell lines, but not in others. In all experiments, lytic viral protein expression by flow cytometry correlated with production of viral particles in culture supernatants. In summary, we found that corticosteroids were limited inducers of KSHV reactivation in latently infected cells. Thus, our findings suggest that corticosteroids do not enhance the incidence and severity of KS in transplant recipients by direct cellular effects on KSHV reactivation. J. Med. Virol. 66:378‐383, 2002. © 2002 Wiley‐Liss, Inc.
Importance of C‐terminus of herpes simplex virus type 1 thymidine kinase for maintaining thymidine kinase and acyclovir‐phosphorylation activities
Authors: Saijo Masayuki , Suzutani Tatsuo , Niikura Masahiro , Morikawa Shigeru , Kurane Ichiro 
Published: August 2002

AbstractWe previously isolated an acyclovir (ACV)‐resistant herpes simplex virus type 1 (HSV‐1), strain TAR, from a child with Wiskott‐Aldrich syndrome. An acyclovir‐sensitive HSV‐1, strain TAS, had been isolated from the same patient before the isolation of HSV‐1 TAR. The TK protein of ACV‐sensitive HSV‐1 TAS was composed of 376 amino acids, while that of HSV‐1 TAR was composed of 407 amino acids with altered amino acid residue between positions 355–407. The elongation of TK was caused by a single nucleotide deletion of cytosine from a homopolymer stretch of 4 cytosine residues between positions 1061–1064. There was no viral TK activity in HSV‐1 TAR‐infected Vero cells, indicating the importance of the C‐terminal portion of TK protein from positions 355–376. Recombinant TK polypeptides with amino acid deletions at the C‐terminus were prepared, and TK and ACV‐phosphorylation activities were examined. Deletion of 5 and 6 amino acids from the C‐terminus of the TK polypeptide of HSV‐1 TAS resulted in a reduction of TK activity by approximately 75% and 100%, respectively. These mutant TK polypeptides did not phosphorylate ACV. These results indicate that amino acid residues from positions 371–376 in the C‐terminal portion of HSV‐1 TK protein are essential for keeping TK and ACV‐phosphorylation activities. J. Med. Virol. 66:388‐393, 2002. © 2002 Wiley‐Liss, Inc.
Human herpesvirus 6 variant a infects human term syncytiotrophoblasts in vitro and induces replication of human immunodeficiency virus type 1 in dually infected cells
Authors: Csoma Eszter , Bácsi Attila , Liu Xiangdong , Szabó Judit , Ebbesen Peter , Beck Zoltán , Kónya József , Andirkó István , Nagy Etelka , Tóth Ferenc D. 
Published: August 2002

AbstractHuman herpesvirus 6 (HHV‐6) and human immunodeficiency virus type 1 (HIV‐1) may interact during transplacental transmission of HIV‐1. The placental syncytiotrophoblast layer serves as the first line of defense of the fetus against viruses. Patterns of replication of HHV‐6 variant A (HHV‐6A) and HIV‐1 were analyzed in singly and dually infected human term syncytiotrophoblast cells cultured in vitro. For this purpose, the GS strain of HHV‐6A and the Ba‐L and IIIB strains of HIV‐1 were used. HHV‐6A replication was restricted at the level of early gene products in singly infected syncytiotrophoblasts, whereas no viral protein expression was found in cells infected with HIV‐1 alone. Coinfection of syncytiotrophoblast cells with HHV‐6A and HIV‐1 resulted in production of infectious HIV‐1. In contrast, no enhancement of HHV‐6A expression was observed in cell cultures infected with both viruses. Uninfected syncytiotrophoblast cells were found to express CXCR4 and CCR3 but not CD4 or CCR5 receptors. Infection of syncytiotrophoblasts with HHV‐6A did not induce CD4 expression and had no influence on chemokine receptor expression. Activation of HIV‐1 from latency in coinfected cells was mediated by the immediate‐early (IE)‐A and IE‐B gene products of HHV‐6A. Open reading frames U86 and U89 of the IE‐A region were able to activate HIV‐1 replication in a synergistic manner. The data suggest that in vivo double infection of syncytiotrophoblast cells with HHV‐6A and HIV‐1 could contribute to the transplacental transmission of HIV‐1 but not HHV‐6A. J. Med. Virol. 67:67–87, 2002. © 2002 Wiley‐Liss, Inc.
Glycosaminoglycan‐promoted muscle reinnervation and insulin‐like growth factor‐I levels are affected by anti‐growth hormone‐releasing hormone exposure
Authors: Gorio Alfredo , Citterio Carmen , Muller Eugenio E. , Di Giulio Anna Maria 
Published: August 2002

AbstractThe present study shows that exposure to antibodies to growth hormone‐releasing hormone (GHRH) partially counteracted the promoting effects of treatment with glycosaminoglycans (GAGs) on muscle reinnervation. Sciatic nerve crush was performed in 2‐day‐old rats, and reinnervation of the extensor digitorum longus muscle was monitored. The extent of reinnervation was rather poor in saline‐treated rats, whereas in GAG‐treated rats the extent of muscle reinnervation, the recovery of nerve‐evoked muscle twitch tension, and the number of motor neurons reinnervating the extensor digitorum longus muscle were greatly enhanced. In addition, treatment with glycosaminoglycans increased markedly insulin‐like growth factor‐I (IGF‐I) levels in denervated muscles. Both types of stimulatory action exerted by GAGs were affected by concomitant exposure to anti‐GHRH, with abolition of IGF‐I muscle increase and a smaller enhancement in muscle reinnervation. J Neurosci. Res. 66:1112–1117, 2001. © 2001 Wiley‐Liss, Inc.
Cytokine signaling in the brain: Putting a SOCS in it?
Authors: Wang Jianping , Campbell Iain L. 
Published: August 2002

AbstractA new family of cytokine‐inducible proteins, termed “suppressors of cytokine signaling” (SOCS), was discovered recently; these proteins function as negative regulators of signaling pathways involved in the cellular actions of many cytokines, growth factors, and hormones. Gene manipulation studies in mice point to the central importance of individual SOCS proteins in maintaining homeostasis by limiting cellular responses to specific cytokines or growth factors in a variety of different physiological systems. Cytokines modulate a wide variety of biological responses in the CNS, so members of the SOCS family might play crucial roles in regulating intracellular signaling by these effectors in both normal and disease states. Although to date studies of the neurobiology of the SOCS family have been limited, we know that many SOCS genes are constitutively expressed in the developing and adult brain, whereas the expression of others, particularly the SOCS1 and SOCS3 genes, can be highly regulated. Furthermore, roles for the SOCS are now evident in the modulation of neuroimmunoendocrine functions affected by a variety of cytokines, including leptin and members of the growth hormone and the interleukin‐6/gp130 superfamilies. Overall, these findings point to the SOCS as likely crucial negative modulators in the temporal and spatial regulation and intensity of cytokine signaling and therefore actions in the CNS. © 2002 Wiley‐Liss, Inc.
Establishment and characterization of immortalized neuronal cell lines derived from the spinal cord of normal and trisomy 16 fetal mice, an animal model of Down syndrome
Authors: Cárdenas Ana María , Allen David D. , Arriagada Christian , Olivares Alexis , Bennett Lori B. , Caviedes Raúl , Dagnino‐Subiabre Alexies , Mendoza Isabel E. , Segura‐Aguilar Juan , Rapoport Stanley I. , Caviedes Pablo 
Published: August 2002

AbstractWe report the establishment of continuously growing cell lines from spinal cords of normal and trisomy 16 fetal mice. We show that both cell lines, named M4b (derived from a normal animal) and MTh (trisomic) possess neurological markers by immunohistochemistry (neuron specific enolase, synaptophysin, microtubule associated protein‐2 [MAP‐2], and choline acetyltransferase) and lack glial traits (glial fibrillary acidic protein and S100). MTh cells were shown to overexpress mRNA of Cu/Zn superoxide dismutase, whose gene is present in autosome 16. We also studied intracellular Ca2+ signals ([Ca2+]i) induced by different agonists in Indo‐1 loaded cells. Basal [Ca2+]i was significantly higher in MTh cells compared to M4b cells. Glutamate (200 μM) and (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylic acid (ACDP) (100 μM) induced rapid, transient increases in [Ca2+]i in M4b and MTh cells, indicating the presence of glutamatergic metabotropic receptors. N‐methyl‐D‐aspartate (NMDA) and kainate, but not alpha‐amino‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA), produced [Ca2+]i rises in both cell types. MTh cells exhibited faster time‐dependent decay phase kinetics in glutamate‐induced responses compared to M4b cells. Nicotine induced a transient increase in [Ca2+]i in M4b and MTh cells, with significantly greater amplitudes in the latter compared to the former. Further, both cell types responded to noradrenaline. Finally, we examined cholinergic function in both cell lines and found no significant differences in the [3H]‐choline uptake, but fractional acetylcholine release induced by either K+, glutamate or nicotine was significantly higher in MTh cells. These results show that M4b and MTh cells have neuronal characteristics and the MTh line shows differences which could be related to neuronal pathophysiology in Down's syndrome. © 2002 Wiley‐Liss, Inc.
Effects of locally administered pentylenetetrazole on nigral single unit activity and severity of dystonia in a genetic model of paroxysmal dystonia
Authors: Fedrowitz Maren , Hamann Melanie , Rehders Jan H. , Richter Angelika , Gernert Manuela 
Published: August 2002

AbstractThe dtsz hamster is a well‐established animal model of idiopathic paroxysmal dystonia. Previous investigations of this mutant have indicated dysfunctions of the γ‐aminobutyric acid (GABA)‐ergic system within the basal ganglia. Systemic administration of the central stimulant pentylenetetrazole (PTZ) aggravated dystonia at subconvulsant doses, whereas GABA‐mimetic drugs have beneficial effects in dtsz hamsters. GABA mimetics also provide clinical benefit in humans with idiopathic paroxysmal dystonia. The spontaneous discharge rates of substantia nigra pars reticulata (SNr) neurons was unaltered in anesthetized dtsz hamsters, but systemic application of subconvulsant doses of PTZ caused significantly greater increases of discharge rates in dystonic hamsters compared with nondystonic controls. The present study tested the hypothesis that SNr neurons are more sensitive to local application of PTZ in dtsz hamsters than in nondystonic hamsters. PTZ applied locally by pressure injection at 2, 3, and 5 mM to the SNr during in vivo single unit recordings revealed a dose‐dependent increase of SNr discharge rates in mutants and controls relative to predrug rates, with a significantly greater increase in mutants at 3 mM PTZ. To examine the functional relevance of the increased susceptibility of SNr neurons to PTZ in mutants, the effects of PTZ on severity of dystonia were investigated after microinjections into the SNr of freely moving dtsz hamsters. Bilateral nigral microinjection of 40 ng PTZ did not aggravate dystonia but exerted moderate antidystonic effects. Therefore, the previous findings of prodystonic effects of systemic administration of PTZ in dtsz hamsters are related to extranigral effects rather than to the elevation of nigral discharge rates in response to systemic, or locally applied, PTZ. The greater susceptibility of neurons within the SNr to PTZ suggests dysfunctions of the GABAA receptor in dtsz mutants. © 2002 Wiley‐Liss, Inc.
Cell death in the superficial dorsal horn in a model of neuropathic pain
Authors: Whiteside G.T. , Munglani R. 
Published: August 2002

AbstractThe aims of this study were to investigate the occurrence of apoptotic cell death in the dorsal horn of the adult rat spinal cord following chronic constriction injury (CCI) to the sciatic nerve and to correlate this with behavioural responses. Six groups of six rats were used as follows: 1) CCI, 2) CCI, 3) MK801 + CCI, 4) axotomy, 5) sham, and 6) naive. Group 1 animals were behaviourally tested for thermal hyperalgesia 8 days following surgery and sacrificed and the spinal cords removed and frozen. The rest of the groups underwent the same procedure 14 days following surgery. The lumbar region of the spinal cord was cryosectioned and the incidence of apoptotic cells investigated using the TUNEL technique plus Hoechst double labelling. By 8 days post‐CCI, hyperalgesia had developed in the ipsilateral paw, which was still present 14 days after the injury compared to the contralateral paw and naive and sham animals. Preemptive MK‐801 prevented the onset of hyperalgesia. Significant numbers of apoptotic cells were present in the ipsilateral dorsal horn of the spinal cord 8 and 14 days following CCI compared to the contralateral side and to naive and sham animals. Preemptive treatment with MK‐801 reduced the extent of apoptosis resulting from CCI to the level seen in control animals. This study demonstrates that cells undergo apoptosis as a result of CCI simultaneous with the occurrence of hyperalgesia. Furthermore, MK‐801 prevents the onset of hyperalgesia and reduces the extent of apoptotic cell death, suggesting, perhaps, that apoptosis contributes to the initiation/maintenance of hyperalgesia. J. Neurosci. Res. 64:168–173, 2001. © 2001 Wiley‐Liss, Inc.