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Results for “host factor”

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PubMed2003

TIP, a novel host factor linking callose degradation with the cell-to-cell movement of Potato virus X.

The cell-to-cell movement of Potato virus X (PVX) requires four virus-encoded proteins, the triple gene block (TGB) proteins (TGB25K, TGB12K, and TGB8K) and the coat protein. TGB12K increases the plasmodesmal size exclusion limit (SEL) and may, therefore, interact directly with components of the cell wall or with plant proteins associated with bringing about this change. A yeast two-hybrid screen using TGB12K as bait identified three TGB12K-interacting proteins (TIP1, TIP2, and TIP3). All three TIPs interacted specifically with TGB12K but not with TGB25K or TGB8K. Similarly, all three TIPs interacted with beta-1,3-glucanase, the enzyme that may regulate plasmodesmal SEL through callose degradation. Sequence analyses revealed that the TIPs encode very similar proteins and that TIP1 corresponds to the tobacco ankyrin repeat-containing protein HBP1. A TIP1::GFP fusion protein localized to the cytoplasm. Coexpression of this fusion protein with TGB12K induced cellular changes manifested as deposits of additional cytoplasm at the cell periphery. This work reports a direct link between a viral movement protein required to increase plasmodesmal SEL and a host factor that has been implicated as a key regulator of plasmodesmal SEL. We propose that the TIPs are susceptibility factors that modulate the plasmodesmal SEL.

Amino Acid Sequence↗

PubMed2004

Chlamydia trachomatis serovar E isolates from patients with different clinical manifestations have similar courses of infection in a murine model: host factors as major determinants of C trachomatis mediated pathogenesis.

BACKGROUND: Some investigators have proposed an association between certain Chlamydia trachomatis serovars and the clinical course of infection in humans. A recent study of over 1100 patients with culture confirmed and serotyped C trachomatis urogenital infection detected no such association. AIMS: To corroborate these results using a murine model of female genital tract infection. METHODS: Various parameters of infection were assessed in mice intravaginally infected with human genital isolates of C trachomatis serovar E from four cases with either a clear symptomatic or asymptomatic clinical course in both the patient and their partner. RESULTS: No differences were seen among the strains in the incidence or duration of infection, polymorphonuclear granulocyte responses, or upper genital tract progression. CONCLUSIONS: An investigation to determine the correlation between the clinical manifestations of different isolates of C trachomatis serovar E in humans and certain parameters of microbial pathogenesis in a mouse model failed to reveal an association between the measured parameters and the tendency of serovar E to produce symptomatic versus asymptomatic infections in humans. These findings suggest that differences in the clinical course of infection in humans seen with these strains may be more related to host factors than to genetic variation among strains.

Animals↗

PubMed2006

SerpinB2 is an inducible host factor involved in enhancing HIV-1 transcription and replication.

The serine protease inhibitor SerpinB2 (plasminogen activator inhibitor-2) is a major product of activated monocytes and macrophages and is substantially induced during most inflammatory processes. Distinct from its widely described extracellular role as an inhibitor of urokinase plasminogen activator, SerpinB2 has recently been shown to have an intracellular role as a retinoblastoma protein (Rb)-binding protein that inhibits Rb degradation. Here we show that HIV-1 infection and gp120 treatment of human peripheral blood mononuclear cells resulted in induction of SerpinB2. Furthermore, SerpinB2 expression in THP-1 monocyte/macrophage, Jurkat T, and HeLa cell lines increased replication of HIV-1 and enhanced transcription from the HIV-1 long terminal repeat (LTR) promoter by 3-10-fold. Increased HIV-1 gene expression and transcription was also observed in activated macrophages from SerpinB2+/+ mice compared with macrophages from SerpinB2-/- mice. The SerpinB2-mediated elevation of Rb protein levels appeared to be responsible for enhancing transcription from the core promoter region of the LTR by relieving HDM2-mediated inhibition of Sp1 and/or by increasing the Sp1/Sp3 expression ratios. This is the first report associating HIV-1 replication with SerpinB2 expression and illustrates that SerpinB2 is a potentially important inducible host factor that significantly promotes HIV-1 replication.

Animals↗

PubMed1996

Modulation of DNA binding in vivo by specific humoral immunological response: a novel host factor in environmental carcinogenesis?

To investigate the possible modulatory effect of the immune response induced by recurrent carcinogen exposure, a specific humoral immune response toward 2-acetylaminofluorene (2-AAF) was elicited in Swiss mice with repeated intraperitoneal injections of a 2-AAF-gelatin conjugate. The immunization procedure resulted in the production of specific anti-2-AAF antibodies in all treated animals. Groups of immunized and nonimmunized mice were subsequently fed 2-AAF pelleted in the diet at 50 and 150 ppm for 4 weeks. At the end of 2-AAF administration, animals were sacrificed and the content of 2-AAF-adducts in liver DNA was determined by enzyme-linked immunoadsorbent assay using a polyclonal rabbit antiserum. The comparison of the adducts levels in immunized and nonimmunized mice (receiving either the vehicle or the adjuvant alone during pretreatment) demonstrates a highly significant (p < 0.001) difference among groups, with far lower adduct levels in immunized animals. No significant difference in food consumption or liver metabolic activities was observed among experimental groups, suggesting the absence of external bias. The mechanism underlying the result observed is not yet clear; however, the experimental data strongly suggest that the specific immunological response induced by recurrent carcinogen exposure may exert a modulatory effect and act as a relevant host factor in chemical carcinogenesis.

2-Acetylaminofluorene↗

PubMed2005

Down-regulation of epithelial IL-8 responses in Helicobacter pylori-infected duodenal ulcer patients depends on host factors, rather than bacterial factors.

Helicobacter pylori infection is one of the most common gastrointestinal infections worldwide. Although the majority of the infected individuals remain asymptomatic carriers of the bacteria, approximately 15% develop peptic ulcers, which are most prevalent in the duodenum. H. pylori induce a vigorous immune response which, however, fails to clear the infection. Instead, the chronic inflammation that arises in the infected gastroduodenal mucosa may be involved in the development of H. pylori-associated peptic ulcers. We have previously shown that duodenal ulcer (DU) patients have a significantly lower epithelial cytokine, e.g. IL-8, response in the duodenum than asymptomatic (AS) carriers. In this study we have further investigated the mechanisms behind this finding, i.e. whether it can be explained by bacterial factors, down-regulation of epithelial cytokine production by regulatory T cells, or an impaired ability of the duodenal epithelium in DU patients to produce cytokines. Gastric AGS, and intestinal T84 epithelial cell lines were stimulated with H. pylori strains isolated from DU patients and AS carriers, respectively. All strains were found to induce comparable cytokine and cytokine receptor expression in epithelial cells. Regulatory T cells (CD4+ CD25(high)), isolated from human peripheral blood and cocultured with H. pylori stimulated AGS cells, were found to slightly suppress H. pylori-induced epithelial cytokine production. Furthermore, primary cultures of duodenal epithelial cells from DU patients were found to produce markedly lower amounts of cytokines than epithelial cells isolated from AS carriers. These results suggest that the lower epithelial cytokine responses in the duodenum of DU patients, which may be of importance for the pathogenesis of H. pylori-induced duodenal ulcers, most likely can be explained by host factors, i.e. mainly a decreased ability of the duodenal epithelium to produce cytokines, but possibly partly also down-regulation by regulatory T cells.

CD4-Positive T-Lymphocytes↗

PubMed2005

Viral and host factors in early hepatitis C virus infection.

Since 1980, the Transfusion-transmitted Viruses Study (TTVS) (1974-1980) has continued to maintain its computerized database and stored sera to enable ongoing study of new transfusion events since the 1970s. Most recently, we have used this resource to study parameters of acute hepatitis C virus (HCV) infection among 94 donor-recipient pairs in which there was transmission. In addition, frequent recipient observations permitted further characterization of the early phase of the infection's course. Donor RNA load ranged from 3.7 to 3,160,000 IU/mL. Onset of recipient viremia was judged from a total of 67 sera collected during the 4th through 8th days posttransfusion; only 2 of the 67 sera were still RNA nonreactive by that time. The recipients' latent periods to an alanine aminotransferase (ALT) elevation of > or =90 IU/L ranged from 6 to 112 days (median, 46 days) and was shorter with higher donor RNA levels. Descriptors of the recipient's illness showed several strongly positive and negative correlations. The latent period tended to be shorter in the 37% of cases that were clinically overt. Attributes of donors with genotypes 1 and non-1 and subtypes 1a and 1b did not differ significantly. Recipients with genotype 1 strains had shorter latent intervals than non-1 strains. On multivariate analysis, latent period was significantly associated (negatively) only with the highest ALT level during the first 120 days of follow-up (P = .014). In conclusion, host factors are more important determinants of acute HCV infection dynamics than virus-associated factors.

Adult↗

PubMed1995

Fulminant hepatitis associated with hepatitis B virus e antigen-negative infection: importance of host factors.

The precore stop-codon variant of hepatitis B virus (HBV) has been implicated in fulminant hepatitis. The precore/core regions of such variants from two sets of patients with interpartner transmission resulting in fulminant hepatitis in the contact, were sequenced to establish whether further sequence variations in the core region are specifically associated with the fulminant disease. In both sets of patients, there was sequence diversity of the precore/core region from the wild type, leading to numerous amino acid substitutions in the core region. Between the infecting source and the contact, there was only one amino acid change in one set of patients and none in the other. In addition, in the second set of patients, serum samples from four different time points were investigated. Sequence data showed no variation in each patient at the nucleotide level in the core region, even in the case of the source, who was followed for 3 years. In this same pair of subjects, the remainder of the genome was sequenced and was identical at the nucleotide level. Therefore, it appears that, at least in some cases of fulminant hepatitis caused by infection with the precore variant, the nucleotide sequence of the patient with fulminant hepatitis is identical to that observed in the asymptomatic source of infection. These data indicate that the severity and outcome of infection in such cases are unrelated to any additional variation in the entire HBV genome, and that the changed clinical picture is dependent on host factors, possibly the HLA environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1982

Studies of host factors in carcinogenesis using cultured human tissues and cells.

Recent progress in the development of conditions for culturing epithelial tissues and cells from adult humans has provided cancer researchers with an opportunity to investigate directly the various facets of carcinogenesis in human cells. Studies of activation and deactivation of several classes of chemical carcinogens have revealed that the metabolic pathways and the predominant adducts formed with DNA are generally similar in humans and experimental animals. Wide quantitative interindividual differences are found in humans and other outbred animal species. When the metabolic capabilities of specimens from different levels of biological organization are compared, the profile of benzo[a]pyrene metabolites is similar in cultured tissues and cells, but subcellular fractions, e.g., microsomes, produce a qualitatively and quantitatively aberrant pattern. To test the interactive effects of cell types in the metabolic activation of carcinogens and to assess further interindividual differences among people, human tissue- and cell-mediated mutagenesis assays have been developed. The fact that terminally differentiated cells such as pulmonary alveolar macrophages can activate benzo[a]pyrene and mediate an increase in frequencies of mutations and sister chromatid exchanges in cocultivated 'detector' cell populations, i.e., Chinese hamster V79 cells, suggests that non-target cells of chemical carcinogens may play an important role in the activation of environmental carcinogens. Malignant transformation of human epithelial and fibroblastic cells in vitro has been accomplished by several research groups. Asbestos, a cocarcinogenic agent in bronchogenic carcinogenesis, has been found to induce polyploid epithelial lesions with atypical cells in human bronchial explants. Carcinogenesis studies using cultured human tissues and cells are providing new insights into the mechanisms of carcinogenesis and are useful in identifying host factors that influence individual risk to environmental carcinogens.

Biotransformation↗

PubMed1988

Debrisoquine hydroxylation phenotype, acetylation phenotype, and ABO blood groups as genetic host factors of lung cancer risk.

Bronchogenic carcinoma is closely associated with cigarette smoking although additional environmental or individual factors might regulate a person's susceptibility to that disease. To further define such risk factors, the prevalence of the genetic debrisoquine 4-hydroxylation deficiency was determined before therapeutic intervention in 270 lung cancer patients. Nineteen homozygous carriers of this defect (poor metabolizers) were found (7.0%, 95% confidence limits 4.3%-10.8%), a number being lower than 30 out of 270 reference patients (11.1%, 95% confidence limits 7.6%-15.5%). The odds ratio of 0.61 was of marginal statistical significance (P = 0.067). Subdividing the collective according to histology revealed a trend towards underrepresentation of poor metabolizers especially among patients with adenocarcinoma (1 out of 37, P = 0.086) and among young patients not older than 50 years (none out of 32, P = 0.028). All poor metabolizers (PMs) in the cancer group were smokers. In 18 patients the phenotype assignment was confirmed by a second test several weeks after surgical or other treatment. In 220 of the lung cancer patients the N-acetyltransferase polymorphism was evaluated by means of the molar ratio of 5-acetylamino-6-formylamino-3-methyluracil and 1-methylxanthine in urine after ingestion of caffeine (coffee). There were 111 (50.5%) slow acetylators and 109 (49.5%) fast acetylators. A statistically significant clustering of either phenotype after stratification according to histology, or debrisoquine hydroxilator status was lacking. Moreover, there was no difference in the ratio of both phenotypes as compared to the reference collective of 245 patients (53.5% slow and 46.5% fast acetylators). As a third genetic host factor the AB0 blood group frequencies were evaluated in 263 lung cancer patients. The frequency ratio of A/O was significantly higher as compared to 41,423 blood donors (odds ratio 1.37, 95% confidence limits 1.02-1.84, P less than 0.05). A/O tended to be especially high in young patients not older than 50 years. The ratio B/O in bronchial cancer was significantly higher than expected. The results suggest that the debrisoquine hydroxilator status might have an impact on an individual's susceptibility to lung cancer. This association is either a weak one and/or is restricted to certain histological cancer types or to patients with certain characteristics. The acetylator phenotype could not be established as a risk factor, whereas AB0 blood groups seem to influence lung cancer susceptibility.

ABO Blood-Group System↗

PubMed2003

Host factor titration by chromosomal R-loops as a mechanism for runaway plasmid replication in transcription termination-defective mutants of Escherichia coli.

Two Escherichia coli genes, rnhA and recG, encode products that disrupt R-loops by hydrolysis and unwinding, respectively. It is known that the propensity for R-loop formation in vivo is increased during growth at 21 degrees C. We have identified several links between rnhA, recG, and R-loop-dependent plasmid replication on the one hand, and genes rho and nusG involved in factor-dependent transcription termination on the other. A novel nusG-G146D mutation phenocopied a rho-A243E mutation in conferring global deficiency in transcription termination, and both mutants were killed at 21 degrees C following overexpression of rnhA(+). Mutant combinations rnhA-nusG or recG-rho were synthetically lethal at 21 degrees C, with the former being suppressed by recG(+) overexpression. rho and nusG mutants were killed following transformation with plasmids such as pACYC184 or pUC19 (which have R-loop replication intermediates) even at 30 degrees C or 37 degrees C, and the lethality was correlated with greatly increased content of supercoiled monomer species of these and other co-resident R-loop-dependent plasmids. Plasmid-mediated lethality in the mutants was suppressed by overexpression of rnhA(+) or recG(+). Two additional categories of trans-acting suppressors of the plasmid-mediated lethality were identified whose primary effects were, respectively, a reduction in plasmid copy number even in the wild-type strain, and a restoration of the proficiency of in vivo transcription termination in the nusG and rho mutant strains. The former category of suppressors included rom(+), and mutations in rpoB(Q513L), pcnB, and polA, whereas the latter included a mutation in rho (R221C) and several non-null mutations (E74K, L26P, and delta64-137) in the gene encoding the nucleoid protein H-NS. We propose that an increased occurrence of chromosomal R-loops in the rho and nusG mutants leads to titration of a cyloplasmic host factor(s) that negatively modulates the stability of plasmid R-loop replication intermediates and consequently to runaway plasmid replication.

Bacterial Proteins↗

PubMed2006

[Host factors that regulate the intercellular dynamics of HIV-1 genome during the early phase of infection].

An interplay or battle between virus and its host has been observed within a single cell. Upon an infection with retroviruses including human immunodeficiency virus type 1 (HIV-1), the viral genome is subjected to several processes that include uncoating, reverse transcription of the viral genomic RNA into a cDNA copy, transport of this cDNA into the nucleus, and integration of the cDNA into the host chromosome. Antiretroviral restriction factors such as TRIM5 alpha and APOBEC3G have been recently identified. In addition, nuclear membrane protect host chromosomal DNA against incoming viral genome. For successful retroviral infection, viral genome must overcome these cellular barriers to establish proviral state, in which viral cDNA was stably integrated into host chromosomal DNA. In this review, I would summarize the host factors that regulate the intercellular dynamics of HIV-1 genome during the early phase of infection, especially focusing on factors interacting with HIV-1 integrase and the preintegration complex.

APOBEC-3G Deaminase↗

PubMedDate not supplied

Host factors and susceptibility to influenza A infection: the effect of ABO blood groups and HL-A antigens.

The effect of two host genetic factors on the outcome of influenza A infections has been examined, ABO blood groups and HL-A antigens. A significantly higher proportion of blood group B subjects was found to have serological evidence of infection with epidemic influenza despite a high incidence of residual antibody among the volunteers. No difference was observed in the ability of subjects of different blood groups to seroconvert after receiving two doses of live attenuated influenza A vaccine, but a significantly higher proportion of blood group A vaccines seroconverted after receiving their first dose of vaccine. The association between HL-A type BW16 and resistance to infection with influenza could not be confirmed. The results are discussed in terms of an indirect association between susceptibility to influenza infection and the two host genetic factors.

ABO Blood-Group System↗

PubMed2002

The interplay between environmental and host factors during an outbreak of visceral leishmaniasis in eastern Sudan.

Parasitic diseases, including human visceral leishmaniasis, are multifactorial. Factors that are expected to play an important role in the parasite-human interaction are exposure, parasite "virulence" and host resistance factors. In populations exposed to Leishmania donovani most subjects do not allow the parasites to establish themselves or remain asymptomatic. Some individuals, however, fail to control parasite expansion and dissemination and develop a visceral disease. We report here the results of a longitudinal survey whose aims were to identify risk factors underlying visceral leishmaniasis (VL) susceptibility during an outbreak that occurred in a Sudanese village between 1995 and 1999. Most of the 660 subjects (90%) living in the central district were exposed to Leishmania and 20.9% (n = 138), mostly teenagers, developed VL. VL cases increased markedly in adults late in the outbreak, suggesting some changes in adult resistance status or in Leishmania "virulence" during the epidemic. Age and ethnic origin of the patients were the most important critical risk factors to account for the distribution of the VL cases that were recorded during the whole epidemic. This and the high frequency of VL in certain families suggest that host genetic factors played an important role in shaping the outbreak in this village. However, environmental factors (the presence of cows and neems in the households) that increase/decrease exposure to the parasite had significant effects on the distribution of VL cases in the village in the first phase of the outbreak.

Adult↗

PubMed2004

Posthodiplostomum cuticola (Digenea: Diplostomatidae) in intermediate fish hosts: factors contributing to the parasite infection and prey selection by the definitive bird host.

Infection parameters of Posthodiplostomum cuticola, a digenean parasite with a complex life-cycle, were investigated in fish (the second intermediate host) from 6 floodplain water bodies over 2 years. A broad range of factors related to abiotic characteristics of localities, density of the first intermediate (planorbid snails) and definitive (wading birds) hosts and fish community structure were tested for their effects on P. cuticola infection in juvenile and adult fish. Characters of the littoral zone and flood duration were found to be important factors for the presence of the first intermediate and definitive hosts. Visitation time of definitive bird hosts was also related to adult fish host density. Localities with P. cuticola infected fish were visited by a higher number of bird species. Infection of P. cuticola in fish and similarities in infection among fish host assemblages were correlated with fish host density and fish species composition. Parasite infection in both adult and juvenile fishes was associated with the slope of the bank and the bottom type, in particular in juvenile fish assemblages with snail host density. We conclude that habitat characteristics, snail host density and fish community structure contribute significantly to P. cuticola infection in fish hosts.

Animals↗

PubMed1998

Increased urinary polyamine excretion in unselected cancer patients related to host factors.

Unselected patients with solid malignant tumours were investigated in order to determine whether they displayed elevated urinary excretion of polyamines; and if so, whether polyamine excretion in such patients predicts disease progression, or is secondary to host and systemic factors. Thirty-eight male and female patients with generalized solid, mainly gastrointestinal, malignant tumours were investigated. Ten male patients operated on for infrarenal aortic aneurysms and 15 otherwise healthy male and female patients hospitalized for minor surgical procedures served as reference patients, representing individuals with and without metabolic stress. Urine samples were collected from all patients during 24 h for measurement of both total and individual excretion of polyamines during three consecutive days. Polyamine excretion was not significantly increased in cancer patients when compared by analysis of variance among the three patient groups. However, polyamine excretion was significantly elevated in both cancer and stressed, non-cancer patients compared with patients without stress (p < 0.05). A multivariate analysis indicated that plasma protein and albumin concentrations, abnormal liver function tests and liver metastasis predicted variation in polyamine excretion in cancer patients (p < 0.01), but this was unrelated to survival. Our results demonstrate that increased polyamine excretion in cancer patients is related more to host factors than to tumour growth itself.

Aged↗

PubMed2002

The role of bacterial virulence and host factors in patients with Escherichia coli bacteremia who have acute cholangitis or upper urinary tract infection.

We studied the pathogenic role of host and Escherichia coli virulence factors in the development of E. coli bacteremia in patients with acute cholangitis (AC) or upper urinary tract infection (UTI). Isolates recovered from 75 adult patients consecutively admitted to the hospital with E. coli bacteremia caused by AC (n=24) or upper UTI (n=51) were evaluated, as were 30 fecal strains isolated from healthy control individuals. Virulence genes of E. coli were detected by polymerase chain reaction analysis, including papG genes (classes I-III), sfa/foc, fimH, afa, hlyA, cnf1, and iutA. Our results show that biliary tract obstruction and urinary tract obstruction are important host factors for the development of E. coli bacteremia in patients with AC and upper UTI, respectively. With regard to E. coli virulence factors, the papG class II gene might play a more important role in the development of E. coli bacteremia in patients with upper UTI than in those with AC.

Acute Disease↗

PubMed2006

[Recurrence of hepatitis C virus (HCV) infection after liver transplantation for HCV-related disease: host factors and viral factors implicated in the occurrence and the severity of HCV recurrence].

Cirrhosis due to chronic infection by hepatitis C virus (HCV), associated or not to a primary hepatocarcinoma, has become the first indication of liver transplantation. Graft reinfection by HCV is considered to be systematic while its prognosis is variable from one patient to another. A better knowledge of factors implicated in the occurrence and severity of hepatitis C recurrence is crucial in order to make optimal patients' monitoring. This article aims to present available data in this field, clarifying the role of viral factors (viral load, genotype, evolution of viral quasispecies) and host-related factors (immune response) which could take part in the development of hepatitis C recurrence.

Carcinoma, Hepatocellular↗

PubMed1997

Strongly reduced phage Qbeta replication, but normal phage MS2 replication in an Escherichia coli K12 mutant with inactivated Qbeta host factor (hfq) gene.

RNA phage production was observed in Escherichia coli hfq mutant strains transformed with plasmids containing genomic cDNA of phages Qbeta or MS2. Qbeta production was reduced 5000-fold in an insertional mutant containing an omega cassette in the middle of hfq, but was unaffected in a mutant with the cassette near the end of hfq. The insertions had no effect on MS2 replication.

Carrier Proteins↗