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PubMed1992

Host factors and acute lower respiratory infections in pre-school children.

The relationship between certain host-related variables and the short-term outcome of hospitalization for severe acute lower respiratory infections was studied prospectively in a cohort of 103 pre-school Nigerian children. The respective mean ages of those with bronchiolitis and croup were 3.2 months and 18.9 months while the corresponding M:F ratios were 2.5:1 and 1:1. It was highly significant that all the eight children that died were malnourished (P less than 0.01). Furthermore, malnourished subjects with pleural effusion, in whom bacteraemia was common, stayed longest in hospital while subjects with bronchiolitis and croup, in whom malnutrition was distinctly uncommon, had the shortest duration of admission. Multiple microbial identifications and bacteraemia were common in malnourished subjects with ALRI. Mortality was significantly higher in older children (P less than 0.05), but sex, immunization/breast-feeding status and co-existing measles or pertussis, were individually neither related to the admission outcome nor the duration. It is concluded that malnutrition is a strong predictor of ALRI-related death in the pre-school child. The significance of bacteraemia and multiple microbial identifications in malnourished children, and the ARI-control implications of the study are discussed.

Acute Disease↗
PubMed2006

Identification of essential host factors affecting tombusvirus RNA replication based on the yeast Tet promoters Hughes Collection.

To identify essential host genes affecting replication of Tomato bushy stunt virus (TBSV), a small model plant virus, we screened 800 yeast genes present in the yeast Tet promoters Hughes Collection. In total, we have identified 30 new host genes whose down-regulation either increased or decreased the accumulation of a TBSV replicon RNA. The identified essential yeast genes are involved in RNA transcription/metabolism, protein metabolism/transport, or other cellular processes. Detailed analysis of the effects of some of the identified yeast genes revealed that they might affect RNA replication by altering (i) the amounts/functions of p33 and p92(pol) viral replication proteins, (ii) the standard 10 to 20:1 ratio between p33 and p92(pol) in the viral replicase, (iii) the activity of the tombusvirus replicase, and (iv) the ratio of plus- versus minus-stranded RNA replication products. Altogether, this and previous genetic screening of yeast (Panavas et al., Proc. Natl. Acad. Sci. USA 102:7326-7331, 2005) led to the identification of 126 host genes (out of approximately 5,600 genes that represent approximately 95% of all the known and predicted yeast genes) that affected the accumulation of tombusvirus RNA.

Genes, Essential↗
PubMed2005

The role of Candida albicans NOT5 in virulence depends upon diverse host factors in vivo.

We previously identified Candida albicans Not5p as an immunogenic protein expressed during oropharyngeal candidiasis (OPC). In this study, we demonstrate that C. albicans NOT5 reverses the growth defects of a Saccharomyces cerevisiae not5 mutant strain at 37 degrees C, suggesting that the genes share at least some functional equivalence. We implicate C. albicans NOT5 in the pathogenesis of disseminated candidiasis (DC) induced by intravenous infection among neutropenic and nonimmunosuppressed mice, as well as in that of OPC in mice immunosuppressed with corticosteroids. We find no role in virulence, however, among neutropenic and corticosteroid-suppressed mice with DC resulting from gastrointestinal translocation, nor do we implicate the gene in vulvovaginal candidiasis among mice in pseudoestrus. These findings suggest that the role of NOT5 in virulence depends on the specific in vivo environment and is influenced by diverse factors such as tissue site, portal of entry, and the status of host defenses. NOT5 is necessary for normal adherence to colonic and cervical epithelial cells in vitro, demonstrating that such assays cannot fully replicate disease processes in vivo. Lastly, antibody responses against Not5p do not differ in the sera of patients with OPC, patients with DC, and healthy controls, suggesting that the protein is associated with both commensalism and the pathogenesis of disease.

Animals↗
PubMed2006

Screening of the yeast yTHC collection identifies essential host factors affecting tombusvirus RNA recombination.

RNA recombination is a major process in promoting rapid virus evolution in an infected host. A previous genome-wide screen with the yeast single-gene deletion library of 4,848 strains, representing approximately 80% of all genes of yeast, led to the identification of 11 host genes affecting RNA recombination in Tomato bushy stunt virus (TBSV), a small model plant virus (E. Serviene, N. Shapka, C. P. Cheng, T. Panavas, B. Phuangrat, J. Baker, and P. D. Nagy, Proc. Natl. Acad. Sci. USA 102:10545-10550, 2005). To further test the role of host genes in viral RNA recombination, in this paper, we extended the screening to 800 essential yeast genes present in the yeast Tet-promoters Hughes Collection (yTHC). In total, we identified 16 new host genes that either increased or decreased the ratio of TBSV recombinants to the nonrecombined TBSV RNA. The identified essential yeast genes are involved in RNA transcription/metabolism, in protein metabolism/transport, or unknown cellular processes. Detailed analysis of the effect of the identified yeast genes revealed that they might affect RNA recombination by altering (i) the ratio of the two viral replication proteins, (ii) the stability of the viral RNA, and/or (iii) the replicability of the recombinant RNAs. Overall, this and previous works firmly establish that a set of essential and nonessential host genes could affect TBSV recombination and evolution.

Base Sequence↗
PubMed1999

Neuroendocrine host factors and inflammatory disease susceptibility.

The etiology of autoimmune diseases is multifactorial, resulting from a combination of genetically predetermined host characteristics and environmental exposures. As the term autoimmune implies, immune dysfunction and dysregulated self-tolerance are key elements in the pathophysiology of all these diseases. The neuroendocrine and sympathetic nervous systems are increasingly recognized as modulators of the immune response at the levels of both early inflammation and specific immunity. As such, alterations in their response represent a potential mechanism by which pathologic autoimmunity may develop. Animal models of autoimmune diseases show pre-existing changes in neuroendocrine responses to a variety of stimuli, and both animal and human studies have shown altered stress responses in the setting of active immune activation. The potential role of the neuroendocrine system in linking environmental exposures and autoimmune diseases is 2-fold. First, it may represent a direct target for toxic compounds. Second, its inadequate function may result in the inappropriate response of the immune system to an environmental agent with immunogenic properties. This article reviews the relationship between autoimmune diseases and the neuroendocrine system and discusses the difficulties and pitfalls of investigating a physiologic response that is sensitive to such a multiplicity of environmental exposures.

Animals↗
PubMed1985

Host factors predisposing to anaerobic infections.

Anaerobic bacterial infections of man are typically associated with locally comprised tissues and commonly also with a systemically compromised host. Thus, any condition that interferes with the systemic defence mechanisms of the host and thus predisposes to infection in general, increases the incidence of anaerobic infections also. It is generally true to say that anaerobic infections occur secondary to mechanical disruption of anatomical barriers, usually percutaneous in clostridial infections; in nonclostrial anaerobic infections the disrupted barriers are commonly mucosal surfaces where the offending organisms exist as the dominant part of normal bacterial floras. The most important single factor which enables anaerobes to flourish in the tissues is low oxygen tension which is usually the result in the first instance of a compromised blood supply and poor tissue perfusion. A variety of other predisposing factors may operate in concert, enabling the nonsporing anaerobes to cause a diversity of infective states in many different parts of the body. These host determinants are considered in relation to clostridial, nonclostridial and postsurgical anaerobic sepsis.

Bacteria, Anaerobic↗
PubMed2005

Host factors regulating post-integration latency of HIV.

A recent study has provided important clues towards the identity of the host genes that conspire to promote post-integration latency of human immunodeficiency virus (HIV). Various genes controlling transcription, histone deacetylation and proteasome-mediated protein degradation have emerged as potential players. If the desired, but difficult, goal of complete virus eradication in HIV-infected patients is ever to be realized, the latent reservoir of HIV proviruses must be cleared. Understanding the molecular basis for viral latency is the key first step.

CD4-Positive T-Lymphocytes↗
PubMed1986

Extraintestinal Campylobacter jejuni and Campylobacter coli infections: host factors and strain characteristics.

To determine whether extraintestinal isolates of Campylobacter jejuni and Campylobacter coli are the consequence of unusual host or bacterial characteristics, we studied clinical and bacteriologic features of 24 extraintestinal infections. Common serotypes and auxotypes were present among the extraintestinal isolates. Gastrointestinal isolates were more susceptible to normal human serum than were the systemic isolates; however, the ranges overlapped considerably. Predispositions to systemic spread were present in 52% of patients with extraintestinal infections; isolates from these patients were more often (73%) serum sensitive than were isolates from patients without predispositions (9%; P = .002). By sodium dodecyl sulfate-polyacrylamide gel electrophoresis, no specific protein band was associated with serum resistance, and all isolates of C. jejuni and C. coli had rough-type lipopolysaccharide profiles. Serum susceptibility was inversely correlated with carbohydrate or ketodeoxyoctonate (KDO) fraction of cell weight and directly correlated with KDO:carbohydrate ratio. Our results suggest that either host defects or specific bacterial virulence characteristics, such as serum resistance, possibly related to length of lipopolysaccharide side chain, may be responsible for extraintestinal infections due to C. jejuni and C. coli.

Adolescent↗
PubMed2000

Periodontal disease: bacterial virulence factors, host response and impact on systemic health.

Teeth are coated with a biofilm that contains periodontal pathogens. Pathogens express virulence factors which enable them to invade and replicate within epithelial cells and to invade the underlying connective tissue. This stimulates production of prostaglandins and cytokines that induce tissue loss. In addition, these bacteria have the potential to modulate the course of systemic diseases such as atherosclerosis and to contribute to low birthweight and preterm labor.

Journal Article↗
PubMed1999

Mechanism of DNA replication in eukaryotic cells: cellular host factors stimulating adenovirus DNA replication.

Replication of adenovirus (Ad) DNA depends on interactions between three viral and three cellular proteins. Human transcription factors NFI and Oct-1 recruit the Ad DNA polymerase to the origin of DNA replication as a complex with the Ad protein primer pTP. High affinity and specificity DNA binding to recognition sites in this origin by the transcription factors stimulate and stabilize pre-initiation complex formation to compensate for the low binding specificity of the pTP/pol complex. In this review, we discuss the properties of NFI and Oct-1 and the mechanism by which they enhance initiation of DNA replication. We propose a model that describes the dynamics of initiation and elongation as well as the assembly and disassembly of the pre-initiation complex.

Adenoviridae↗
PubMed2002

Dissemination of Mycobacterium tuberculosis is influenced by host factors and precedes the initiation of T-cell immunity.

We report that dissemination of Mycobacterium tuberculosis in the mouse is under host control and precedes the initiation of T-cell immunity. Nine to eleven days after aerosol inoculation, M. tuberculosis disseminates to the pulmonary lymph nodes (LN), where M. tuberculosis-specific T cells are detected 2 to 3 days thereafter. This indicates that the initial spread of bacteria occurs via lymphatic drainage and that the acquired T-cell immune response is generated in the draining LN. Dissemination to peripheral sites, such as the spleen and the liver, occurs 11 to 14 days postinfection and is followed by the appearance of M. tuberculosis-specific T cells in the lung and the spleen. In all cases studied, dissemination to the LN or the spleen preceded activation of M. tuberculosis-specific T cells in that organ. Interestingly, bacteria disseminate earlier from the lungs of resistant C57BL/6 mice than from the lungs of susceptible C3H mice, and consequently, C57BL/6 mice generate an immune response to M. tuberculosis sooner than C3H mice generate an immune response. Thus, instead of spreading infection, early dissemination of M. tuberculosis may aid in the initiation of an appropriate and timely immune response. We hypothesize that this early initiation of immunity following inoculation with M. tuberculosis may contribute to the superior resistance of C57BL/6 mice.

Animals↗
PubMed1988

Co-factors, host susceptibility, and AIDS: an argument for stress.

Acquired immune deficiency syndrome (AIDS) is perhaps the most serious communicable public-health disease of modern society. The human and societal devastation associated with this disease is tremendous. To date, a retrovirus (HTLV-III) has been implicated in the etiology of AIDS. There remains several critical questions, however, that only a more eclectic approach, certainly with a social science input, can more adequately address. Such questions have to deal with, for example, why are there differential out-comes regarding initiation, progress, and severity of AIDS?Realizing this need, this paper argues for the possible co-factor contribution of stress to host immune suppression and, ultimately, host susceptibility to the AIDS virus and its associated outcomes. A conceptual sociopsychophysiologic model of the entire stress process, ie, from onset, reaction up to and including effect, is presented and discussed. Within the context of the model, stress is viewed as a physiologic reaction and stressors are viewed as initiators of the stress process. The possible stress-AIDS experience is discussed using the model as a conceptual guiding tool. The paper concludes with the need for health educators to educate the general public, at-risk groups, and the medical and associated professions about the nature of stress, or in short, how best to cope with and manage stress within the context of available resources.

Acquired Immunodeficiency Syndrome↗
PubMed2000

The Yersinia protein kinase A is a host factor inducible RhoA/Rac-binding virulence factor.

The pathogenic yersiniae inject proteins directly into eukaryotic cells that interfere with a number of cellular processes including phagocytosis and inflammatory-associated host responses. One of these injected proteins, the Yersinia protein kinase A (YpkA), has previously been shown to affect the morphology of cultured eukaryotic cells as well as to localize to the plasma membrane following its injection into HeLa cells. Here it is shown that these activities are mediated by separable domains of YpkA. The amino terminus, which contains the kinase domain, is sufficient to localize YpkA to the plasma membrane while the carboxyl terminus of YpkA is required for YpkAs morphological effects. YpkAs carboxyl-terminal region was found to affect the levels of actin-containing stress fibers as well as block the activation of the GTPase RhoA in Yersinia-infected cells. We show that the carboxyl-terminal region of YpkA, which contains sequences that bear similarity to the RhoA-binding domains of several eukaryotic RhoA-binding kinases, directly interacts with RhoA as well as Rac (but not Cdc42) and displays a slight but measurable binding preference for the GDP-bound form of RhoA. Surprisingly, YpkA binding to RhoA(GDP) affected neither the intrinsic nor guanine nucleotide exchange factor-mediated GDP/GTP exchange reaction suggesting that YpkA controls activated RhoA levels by a mechanism other than by simply blocking guanine nucleotide exchange factor activity. We go on to show that YpkAs kinase activity is neither dependent on nor promoted by its interaction with RhoA and Rac but is, however, entirely dependent on heat-sensitive eukaryotic factors present in HeLa cell extracts and fetal calf serum. Collectively, our data show that YpkA possesses both similarities and differences with the eukaryotic RhoA/Rac-binding kinases and suggest that the yersiniae utilize the Rho GTPases for unique activities during their interaction with eukaryotic cells.

Actins↗
PubMed2006

Yeast as a model host to dissect functions of viral and host factors in tombusvirus replication.

RNA replication is the central process during the infectious cycles of plus-stranded RNA viruses. Development of yeast as a model host and powerful in vitro assays with purified replicase complexes, together with reverse genetic approaches make tombusviruses, small plant RNA viruses, excellent systems to study fundamental aspects of viral RNA replication. Accordingly, in vitro approaches have led to the identification of protein-RNA interactions that are essential for template selection for replication and assembly of the functional viral replicase complexes. Moreover, genome-wide approaches and proteomics analyses have identified a new set of host proteins that affected tombusvirus replication. Overall, rapid progress in tombusvirus replication has revealed intriguing and complex nature of virus-host interactions, which make robust replication of tombusviruses possible. The knowledge obtained will likely stimulate development of new antiviral methods as well as other approaches that could make tombusviruses useful tools in biotechnological applications.

Proviruses↗
PubMed1993

A specific host factor binds at a cis-acting transcriptionally silent locus required for stability control of yeast plasmid pSR1.

A cis-acting locus, Z, of plasmid pSR1 functions in stable maintenance of the plasmid in the native host, Zygosaccharomyces rouxii. The Z locus was shown to be located in a 482 bp sequence in the 5' upstream region of an open reading frame, P, by subcloning various DNA fragments in a plasmid replicating via the ARS1 sequence of the Saccharomyces cerevisiae chromosome. Northern analysis revealed that the Z region is not transcribed in either the native host Z. rouxii or the heterologous host S. cerevisiae. The Z region is protected from micrococcal nuclease attack in Z. rouxii but not in S. cerevisiae, its protection depending on the product of the S gene encoded by pSR1. Gel retardation assays suggested that a factor present in nuclear extracts of Z. rouxii cells, irrespective of the presence or absence of a resident pSR1 plasmid, binds to a 111 bp RsaI-SacII sequence in the Z region. These findings suggest that a host protein binds to the Z locus and that the S product interacts with this DNA-protein complex and stabilizes pSR1.

Base Sequence↗
PubMed2004

Role of viral and host factors in HCV persistence: which lesson for therapeutic and preventive strategies?

Several lines of evidence support the view that hepatitis C virus is not directly cytopathic for infected host cells and that the immune response plays a central role in the pathogenesis of liver damage. Innate and adaptive immune responses are induced in most individuals infected with hepatitis C virus but are insufficient to eliminate the virus. The mechanisms responsible for this failure are largely unknown but the kinetics of hepatitis C virus replication relative to the priming of the adaptive responses may exert a profound influence on the balance between virus and host. Immediately after hepatitis C virus infection, the virus replicates efficiently, inducing the production of type I interferons. However, the rapid increase in viral replication seems to be ignored by the adaptive immune response, and after a short interval from exposure, viral load can reach levels comparable to those of patients with established persistent infection. The CD8-mediated response shows functional defects, with impaired production of interferon-gamma, low perforin content, decreased capacity of expansion and lysis of target cells. Late appearance and functional defects of T cells in hepatitis C virus infection might be the result of the rapid increase of the viral load that could create the conditions for exhaustion of the adaptive response or reflect an insufficient function of the innate immune response. This possibility is suggested by in vitro studies showing that hepatitis C virus gene products can interfere with the anti-viral activity of type I interferons and natural killer cells as well as with the maturation of dendritic cells. While T-cell defects are reversed in a minority of infected individuals who succeed in controlling the infection, the T-cell impairment becomes progressively more profound as infection progresses to chronicity. In this situation, therapeutic restoration of adaptive responses may represent a rational strategy to obtain resolution of infection and to complement available therapies. The peculiar kinetics of hepatitis C virus replication and T-cell induction soon after infection may have important implications also for the design of protective vaccines since memory responses may not be able to precede the early peak of viral replication. Therefore, vaccines against hepatitis C virus may be unable to prevent infection but may rather be effective in facilitating a self-limited evolution of infection.

Hepacivirus↗