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PubMed1996

Host factors affecting disease transmission.

In prevention of transmission of infectious disease, the host uses a variety of protective mechanisms and can elicit many different responses. Nonspecific defense mechanisms include an intact integument (skin and mucous membranes). The host also can use specialized substances it may secrete, such as mucin or fatty acids to prevent colonization or to inhibit growth of potential pathogens. Specialized surface structures are also used by the host in prevention of disease transmission. These structures include cells composed of keratin and cells with cilia. Additionally, nonspecific protection can be achieved through the actions of the host's nonpathogenic microflora. If these nonspecific barriers to microorganism invasion are breached, other host interactions occur. Complement has many nonspecific actions that may be used to control invasion of microorganisms. PMLs are an additional line of defense the host has available in prevention of infection. These cells are responsible for intracellular killing of pathogens through the use of enzymatic and oxidative mechanisms. The mononuclear phagocyte system allows for elimination of foreign material and debris from the inflammatory reaction. Additionally, the macrophages process and present antigens to T lymphocytes. B lymphocytes differentiate to produce plasma cells, which produce specific antibodies aimed at the invading microorganism. T lymphocytes are involved in the killing of pathogenic microorganisms and in the production of powerful immune modulators known as lymphokines. Fever and inflammation also serve to stimulate reactions aimed at destroying and removing the pathogen from the host system. These factors all play an important role in prevention of disease transmission in a human host.

Antibody Formation↗
PubMed2003

Cleavage of the Pseudomonas syringae type III effector AvrRpt2 requires a host factor(s) common among eukaryotes and is important for AvrRpt2 localization in the host cell.

Many phytopathogenic bacteria use a type III secretion system to deliver type III effector proteins into the host plant cell. The Pseudomonas syringae type III effector AvrRpt2 is cleaved at a specific site when translocated into the host cell. In this study, we first demonstrate that the factor(s) required for AvrRpt2 cleavage is present in extracts from animal and yeast cells, as well as plant cells. The cleavage factor in animal and plant cell extracts was heat labile but relatively insensitive to protease inhibitors. Second, mutational analysis of AvrRpt2 was applied to identify features important for its cleavage. In addition to two of the amino acid residues in the immediate vicinity of the cleavage site, a large part of the region C-terminal to the cleavage site was required when AvrRpt2 was cleaved in animal cell extract. Most of these features were also important when AvrRpt2 was cleaved in plant cells. Third, we investigated the effect of cleavage in interactions of AvrRpt2 with plant cells. Cleavage of AvrRpt2 appeared to be important for proper interactions with Arabidopsis cells that lack the resistance gene product corresponding to AvrRpt2, RPS2. In addition, removal of the region N-terminal to the cleavage site was important for the correct localization of the C-terminal effector region of the protein in the host cell. We speculate that the virulence function of AvrRpt2 requires removal of the N-terminal region to redirect the effector protein to a specific subcellular location in the host cell after translocation of the protein.

Animals↗
PubMed2005

Galectin-1 acts as a soluble host factor that promotes HIV-1 infectivity through stabilization of virus attachment to host cells.

The establishment of HIV type 1 (HIV-1) infection is initiated by the stable attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between virus-encoded gp120 and cell surface CD4, a number of distinct interactions influence binding of HIV-1 to host cells. In this study, we report that galectin-1, a dimeric beta-galactoside-binding protein, promotes infection with R5, X4, and R5X4 variants. Galectin-1 acts as a soluble adhesion molecule by facilitating attachment of HIV-1 to the cell surface. This postulate is based on experiments where galectin-1 rendered HIV-1 particles more refractory to various agents that block HIV-1 adsorption and coreceptor binding (i.e., a blocking anti-CD4, soluble CD4, human anti-HIV-1 polyclonal Abs; stromal cell-derived factor-1alpha; RANTES). Experiments performed with the fusion inhibitor T-20 confirmed that galectin-1 is primarily affecting HIV-1 attachment. The relevance of the present findings for the pathogenesis of HIV-1 infection is provided by the fact that galectin-1 is abundantly expressed in the thymus and lymph nodes, organs that represent major reservoirs for HIV-1. Moreover, galectin-1 is secreted by activated CD8(+) T lymphocytes, which are found in high numbers in HIV-1-positive patients. Therefore, it is proposed that galectin-1, which is released in an exocrine fashion at HIV-1 replication sites, can cross-link HIV-1 and target cells and promote a firmer adhesion of the virus to the cell surface, thereby augmenting the efficiency of the infection process. Overall, our findings suggest that galectin-1 might affect the pathogenesis of HIV-1 infection.

Biological Factors↗
PubMed1998

Effect of integration host factor of RNA II synthesis in replication of plasmid containing orip 15A.

The synthesis rates of the replication control RNAs of plasmid orip15A. RNA I, an inhibitor of replication, and RNA II, the primer, have been determined using lacZ fusion plasmids, hybridization assay, and reverse transcription polymerase chain reaction (RT-PCR) in Escherichia coli integration host factor-positive (IHF+) and -negative (IHF-) strains containing pACYC184 plasmid (orip15A). In the absence of IHF (E. coli IHF-), expression of the lacZ gene from the PRNAII promoter increased by a factor of 4 compared with the E. coli wild type (IHF+). Also, the increase in expression was more pronounced when the IHF protein was mutated in the ihfB gene than in the ihfA gene. For the PRNAII promoter of oripMB1 (pBR322), no significant differences were found in expression of the lacZ gene in he E. coli strains examined. The level of beta-galactosidase expression from the PRNA promoter of orip 15A shows that the absence of functional IHF in the transformed strains has no effect on expression of the lacZ gene. The synthesis RNA II:RNA I ratio obtained in hybridization assays was 2.4 for E. coli IHF+ and 4.4 for E. coli IHF-. Densitometric analysis of RT-PCR products indicates that the relative levels of RNA I in E. coli IHF+ and IHF-, are equal, but the relative level of RNA II in E. coli IHF is about four times higher than in E. coli IHF+. These results indicate that the IHF protein inhibits transcription from the PRNAII promoter of orip15A plasmid.

Artificial Gene Fusion↗
PubMed1981

Host factors and susceptibility to rubella virus infection: the association of HLA antigens.

To examine the role of host-dependent factors to natural rubella infection, the positive rates of HAI antibody according to HLA-A and -B antigens were studied in 93 children, aged 9 to 10, who were exposed only to a recent epidemic (single-exposure group), and in 199 adult females, aged 18 to 23, who were exposed also to a former epidemic (dual-exposure group). Furthermore, the phenotype frequencies of HLA antigens were investigated in seronegative subjects in both groups, as well as in 58 adult female vaccinees, in comparison with those of the Japanese population. The seropositive rates by the HLA antigens, 38.7% and 73.4%, respectively, in each exposure group were found in subjects having some HLA antigens. Several of these candidate HLA antigens varied in phenotype frequencies in seronegative subjects of all three groups from those of the average Japanese. Although a few types were statistically significant, no contradictory findings in susceptibility were obtained among the groups during the study, which suggested strongly that subjects with HLA-Bw51 and -Bw16 are susceptible. In addition, when the seropositive rates were compared in all combinations of HLA-A and -B antigens classified according to expected susceptibility, the positive rates were arranged in order of susceptibility with significant statistical differences in several groups.

Adult↗
PubMed1995

Free amino acids exhibit anthozoan "host factor" activity: they induce the release of photosynthate from symbiotic dinoflagellates in vitro.

Reef-building corals and other tropical anthozoans harbor endosymbiotic dinoflagellates. It is now recognized that the dinoflagellates are fundamental to the biology of their hosts, and their carbon and nitrogen metabolisms are linked in important ways. Unlike free living species, growth of symbiotic dinoflagellates is unbalanced and a substantial fraction of the carbon fixed daily by symbiont photosynthesis is released and used by the host for respiration and growth. Release of fixed carbon as low molecular weight compounds by freshly isolated symbiotic dinoflagellates is evoked by a factor (i.e., a chemical agent) present in a homogenate of host tissue. We have identified this "host factor" in the Hawaiian coral Pocillopora damicornis as a set of free amino acids. Synthetic amino acid mixtures, based on the measured free amino acid pools of P. damicornis tissues, not only elicit the selective release of 14C-labeled photosynthetic products from isolated symbiotic dinoflagellates but also enhance total 14CO2 fixation.

Journal Article↗
PubMed1988

Escherichia coli host factor for site-specific DNA inversion: cloning and characterization of the fis gene.

The Escherichia coli (Es. coli) protein Fis (factor for inversion stimulation) stimulates site-specific DNA inversion of the G segment in phage Mu by binding to a recombinational enhancer. By using synthetic oligonucleotides deduced from the amino-terminal amino acid sequence, we have cloned the gene (termed fis) encoding this specific DNA-binding protein. The DNA sequence shows that the Fis protein is basic and contains 98 amino acids. A helix-turn-helix sequence motif characteristic of many DNA-binding proteins is located at the carboxyl-terminal end of the protein. By marker exchange, we have constructed an insertion mutation of fis. Fis is nonessential for Es. coli growth; however, inversion of the G segment of a Mu prophage was not detected in the fis mutant. The fis gene is located between 71 and 72 min on the Es. coli genetic map.

Amino Acid Sequence↗
PubMed2002

Evaluation of agent and host factors in progression of mycotic keratitis: A histologic and microbiologic study of 167 corneal buttons.

PURPOSE: To evaluate the host and agent factors in the progression of mycotic keratitis through the microbiologic evaluation and histologic study of human corneal buttons obtained at the time of therapeutic keratoplasty. DESIGN: Retrospective noncomparative consecutive case series. MATERIALS: One hundred sixty-seven corneal buttons from 148 patients of microbiologically diagnosed and treated cases of mycotic keratitis who underwent therapeutic keratoplasty between January 1995 and May 1998. METHODS: Therapeutic penetrating keratoplasty, review of microbiologic results, histopathologic and microbiologic evaluation of the corneal buttons of mycotic keratitis MAIN OUTCOME MEASURES: Histologic evaluation of the buttons for morphologic changes, degree and distribution of inflammatory cells, presence or absence of fungal filaments, and their degree and distribution within the corneal buttons. RESULTS: The diagnosis of fungal infection was made on corneal scrapings in 36 cases; whereas in 131 (78%), the fungus was grown in cultures and identified as Aspergillus in 55 (42%), Fusarium in 42 (32%), unidentified hyaline fungi in 22 (17%), dematiaceous (unidentified) in 4 (3%), and others in 8 (6%). The mean interval between diagnosis and keratoplasty was 19 (+/-40) days. From the keratoplasty specimen, the fungus was identified at histologic examination in 127 of 167 (76%) buttons and grown by culture techniques in 76 of 115 (66%) buttons. The fungal species identified in the corneal button were Fusarium in 30 (39%); Aspergillus in 25 (33%); unidentified hyaline in 19 (25%), and others in 2 (3%). Fungus-positive corneal buttons had early surgery (mean, 15 days) compared with fungus-negative (39 days) corneal buttons (P = 0.0005), with 93% fungus positivity in the buttons removed within 2 weeks and 42% after 2 months. In the fungus-positive buttons, there was an inverse correlation between the degree, distribution of inflammatory cells, and fungal filaments (r = -0.255, P = 0.024; r = -0.199, P = 0.027), respectively. The factors necessitating an early keratoplasty were heavy fungal load, deeper penetration of fungus, and possibly insufficient inflammation to combat infection. A granulomatous reaction was noted in the posterior stroma and around the fragmented Descemet's membrane in 23 buttons (13.8%), independent of fungal species. Inflammation was unaffected by elimination of fungus and increasing interval between diagnosis and treatment. CONCLUSIONS: Rapid progression of mycotic keratitis in the early phases is by agent factors such as heavy load and deeper penetration of the fungus, insufficient inflammatory response, and possibly relative ineffectiveness of antifungal agents. Progression in the later phase of mycotic keratitis need not necessarily be agent mediated; it could be either host-modulated, species-related, or drug resistance, thereby suggesting that ideal treatment regimens should include sensitivity-based antifungal therapy aided by in vivo monitoring of fungal filaments.

Adolescent↗
PubMed2001

Host factors involved in West Nile virus replication.

Viruses use cell proteins during many stages of their replication cycles, including attachment, entry, translation, transcription/replication, and assembly. Mutations in the cell proteins involved can cause disruptions of these critical host-virus interactions, which in turn can affect the efficiency of virus replication. These host-virus interactions also represent novel targets for the development of new antiviral agents. The different alleles of the murine Flv gene confer resistance or susceptibility to flavivirus-induced disease and provide a natural mutant system for the study of a host protein that can alter the outcome of a flavivirus infection. Since flaviviruses, such as West Nile virus, replicate in mosquitoes, mammals, and birds during their natural transmission cycles, it is expected that the critical cell proteins used by these viruses will be ones that are highly conserved between divergent host species. Our laboratory has focused on the identification and characterization of the flavivirus resistance gene product and of cell proteins that interact with the 3' terminal regions of the West Nile virus genomic and antigenomic RNAs. The 3' terminal regions of the viral RNAs function as promotors for viral RNA replication. Cell proteins that bind to the viral 3' RNAs were detected by gel shift and UV-induced cross-linking assays. Individual proteins were then purified and partially sequenced. Mutation of a mapped, protein-binding site within the 3' terminal region of the viral RNA in an infectious West Nile virus clone was used to demonstrate the functional importance of one of the cell proteins for efficient West Nile virus replication. Data from additional studies suggested possible roles for this viral RNA-cell protein interaction during the flavivirus replication cycle.

Animals↗
PubMed2001

Dominance of virus over host factors in cross-species activation of human cytomegalovirus early gene expression.

Human cytomegalovirus (HCMV) exhibits a highly restricted host range. In this study, we sought to examine the relative significance of host and viral factors in activating early gene expression of the HCMV UL54 (DNA polymerase) promoter in murine cells. Appropriate activation of the UL54 promoter at early times is essential for viral DNA replication. To study how the HCMV UL54 promoter is activated in murine cells, a transgenesis system based on yeast artificial chromosomes (YACs) was established for HCMV. A 178-kb YAC, containing a subgenomic fragment of HCMV encompassing the majority of the unique long (UL) region, was constructed by homologous recombination in yeast. This HCMV YAC backbone is defective for viral growth and lacks the major immediate-early (IE) gene region, thus permitting the analysis of essential cis-acting sequences when complemented in trans. To quantitatively measure the level of gene expression, we generated HCMV YACs containing a luciferase reporter gene inserted downstream of either the UL54 promoter or, as a control for late gene expression, the UL86 promoter, which directs expression of the major capsid protein. To determine the early gene activation pathway, point mutations were introduced into the inverted repeat 1 (IR1) element of the UL54 promoter of the HCMV YAC. In the transgenesis experiments, HCMV YACs and derivatives generated in yeast were introduced into NIH 3T3 murine cells by polyethylene glycol-mediated fusion. We found that infection of YAC, but not plasmid, transgenic lines with HCMV was sufficient to fully recapitulate the UL54 expression program at early times of infection, indicating the importance of remote regulatory elements in influencing regulation of the UL54 promoter. Moreover, YACs containing a mutant IR1 in the UL54 promoter led to reduced ( approximately 30-fold) reporter gene expression levels, indicating that HCMV major IE gene activation of the UL54 promoter is fully permissive in murine cells. In comparison with HCMV, infection of YAC transgenic NIH 3T3 lines with murine cytomegalovirus (MCMV) resulted in lower (more than one order of magnitude) efficiency in activating UL54 early gene expression. MCMV is therefore not able to fully activate HCMV early gene expression, indicating the significance of virus over host determinants in the cross-species activation of key early gene promoters. Finally, these studies show that YAC transgenesis can be a useful tool in functional analysis of viral proteins and control of gene expression for large viral genomes.

3T3 Cells↗
PubMed2005

Host factors that promote transpososome disassembly and the PriA-PriC pathway for restart primosome assembly.

Initiation of bacteriophage Mu DNA replication by transposition requires the disassembly of the transpososome that catalyses strand exchange and the assembly of a replisome promoted by PriA, PriB, PriC and DnaT proteins, which function in the host to restart stalled replication forks. Once the molecular chaperone ClpX weakens the very tight binding of the transpososome to the Mu ends, host disassembly factors (MRFalpha-DF) promote the dissociation of the transpososome from the DNA template and the assembly of a new nucleoprotein complex. Prereplisome factors (MRFalpha-PR) further alter the complex, allowing PriA binding and loading of major replicative helicase DnaB onto the template promoted by the restart proteins. MRFalpha-PR is essential for DnaB loading by restart proteins even on the deproteinized Mu fork whereas MRFalpha-DF is not required on the deproteinized template. When the transition from transpososome to replisome was reconstituted using MRFalpha-DF and MRFalpha-PR, initiation of Mu DNA replication was strictly dependent upon added PriC and PriA helicase. In contrast, initiation on the deproteinized template was predominantly dependent upon PriB and did not require PriA's helicase activity. The results indicate that transition mechanisms beginning with the transpososome disassembly can determine the pathway of replisome assembly by restart proteins.

Adenosine Triphosphatases↗
PubMed2001

Graft function and survival depend primarily on host factors in compromised recipient models of orthotopic liver transplantation in the rat.

BACKGROUND: Experimental models of liver transplantation use normal recipients, although most patients undergoing liver transplantation suffer from acute or chronic liver failure. This study was designed to analyze the outcome of orthotopic liver transplantation in compromised rat hosts. METHODS: Recipient animals were either rats with D-galactosamine-induced acute or rats with chronic liver failure secondary to common bile duct ligation. Liver damage was evaluated by monitoring enzymes, bilirubin, ammonia levels, prothrombin, thrombin time, and cytokines. In vivo function of hepatocytes and sinusoidal endothelial cells were evaluated by indocyanine green and hyaluronic acid uptake. Transplantation was performed in normal, acute, and chronic liver failure rats at different time points using either freshly harvested or cold-preserved syngeneic livers. RESULTS: Survival with fresh grafts decreased significantly when transplants were performed 48 hr after the induction of acute liver failure. No rats with acute liver failure survived transplantation with grafts stored for 12 or 24 hr although in chronic failure survival was more 80%. Survival of acute liver failure rats receiving 6 hr preserved grafts was 16.6% compared with 83.3% observed with fresh grafts transplanted at the same time point after D-galactosamine injection. Elevated tumor necrosis factor-alpha and interleukin-1beta levels as well as impaired sinusoidal endothelial cell function were detected in acute liver failure rats with 6 h preserved grafts. CONCLUSION: These results suggest that preoperative status and different host factors have a significant effect on outcome and graft function after liver transplantation in rats.

Animals↗
PubMed1986

Drug induced host factors which stimulate growth of residual leukemia in Lewis x Brown Norway F1 (LEW-BN) rats.

Antitumor synergism occurs with two drugs in sequence when the second drug is given at the time of maximal regrowth of residual leukemia and peak humoral stimulatory activity (HSA). To determine if this enhancement relates to a host derived HSA, studies were conducted in Lewis x brown Norway F1 rats bearing brown Norway myelocytic leukemia. A significant cure rate was observed in rats treated initially with 1-beta-D-arabinofuranosylcytosine and then given injections of 10(6) leukemia cells and treated with a second 2-day course of 1-beta-D-arabinofuranosylcytosine in every-8-h s.c. injections in the 6-day period after the initial drug. No effect on survival of the initial drug or of the second drug given at intervals after day 6 was noted. This result is consistent with the efficacy of treatment at the time of peak HSA and tumor growth. The direct effect of HSA on tumor sensitivity to 1-beta-D-arabinofuranosylcytosine was evaluated by 18-h incubations of leukemia and HSA, followed by bioassay. Increased survival and high cure rates were observed when compared with cultured cells in normal serum. These studies support the notion that host derived factors operative during drug induced aplasia stimulate tumor growth and thereby, if the drugs are properly timed, increase sensitivity to cycle active agents.

Animals↗
PubMed1991

A host factor absent from Lactococcus lactis subspecies lactis MG1363 is required for conjugative transposition.

In matings between Lactococcus lactis strains, the conjugative transposons Tn916 and Tn919 are found in the chromosome of the transconjugants in the same place as in the chromosome of the donor, indicating that no transposition has occurred. In agreement with this, the frequency of L. lactis transconjugants from intraspecies matings is the same whether the donor contains the wild-type form of the transposon or the mutant Tn916-int1, which has an insertion in the transposon's integrase gene. However, in intergeneric crosses with Bacillus subtilis or Enterococcus faecalis donors, Tn916 and Tn919 transpose to different locations on the chromosome of the L. lactis transconjugants. Moreover, Tn916 and Tn919 could not be transferred by conjugation from L. lactis and B. subtilis, E. faecalis or Streptococcus pyogenes. This suggests that excision of these elements does not occur in L. lactis. When cloned into E. coli with adjacent chromosomal DNA from L. lactis, the conjugative transposons were able to excise, transpose and promote conjugation. Therefore, the inability of these elements to excise in L. lactis is not caused by a permanent structural alteration in the transposon. We conclude that L. lactis lacks a factor required for excision of conjugative transposons.

Bacillus subtilis↗