Nonpathogenic Phenotype Research Articles

HIV type 2 pathogenicity is not related to subtype in rural Guinea Bissau.

Data from an MRC case-control study in rural Guinea Bissau suggest older HIV-2 carriers (aged 55 to 80 years) appear, over a period of 2 years, to have a mortality similar to that of uninfected controls, whereas in HIV-2 carriers under the age of 55 there is a significantly higher mortality, compared with uninfected controls. Genotyping of viruses from both groups revealed only subtype a to be circulating. Thus, although putative nonpathogenic HIV-2 subtypes have been described in patients from West Africa, these do not appear to be contributing significantly to the nonpathogenic clinical phenotype in this population.

Variation in Cutinase, Esterase, and Chromosome Patterns in Nop Mutants of a Transformed Pathogenic Strain ofPhytophthora capsici

We have designed a strategy to isolate nonpathogenic (Nop) mutants of the Oomycete fungus Phytophthora capsici. This strategy involves direct enrichment or Nop mutants by exposure or mutagenized zoospores to pepper (Capsicum annuum) seedlings and the isolation of germinating zoospores that show chemotaxis but are unable to penetrate the host tissue. After enrichment, 13 Nop mutants were isolated at a frequency of 2-5×10 -2 by N-methyl-N'-nitro-N-nitrosoguanidine mutagenesis. The nonpathogenic phenotype of the mutants was tested by inoculating pepper seedlings as well as pepper fruits with zoospores and mycelia; in all cases no disease symptoms were observed [...]

Pseudomonas solanacearum:Plasmid pJTPS1 Mediates a Shift from the Pathogenic to Nonpathogenic Phenotype

<i>Pseudomonas solanacearum:</i>Plasmid pJTPS1 Mediates a Shift from the Pathogenic to Nonpathogenic Phenotype

Enhanced neurovirulence of tick-borne orbiviruses resulting from genetic modulation

The genome of orbiviruses (Reoviridae family) comprises 10 segments of double-stranded RNA. The fourth largest segment of the tick-borne Kemerovo (KEM) group orbiviruses is the genetic determinant of neurovirulence in experimentally infected mice, and segment 6 determines serotype. Reassortant viruses derived from a cross between two KEM-related viruses, Great Island (GI) and Wexford (WEX), that had the heterotypic gene combination W 4G 6 (segment 4 of WEX virus and segment 6 from GI virus) were nonpathogenic in mice. This apparent genetic modulation of neurovirulence may have resulted from steric interaction between the two outer capsid proteins of nonpathogenic reassortants. Further data are consistent with this hypothesis. Reassortants generated from additional KEM group viruses showed various degrees of enhanced neurovirulence in terms of their PFU/LD5o (ratio of infectivity in cell culture and in mice) and AST max (the average survival time at the highest virus dilution resulting in 100% mortality). Some reassortants were more pathogenic of their parental viruses. The results indicate that the gene determining neurovirulence dictates AST max, and the PFU/LD 50 is a measure of the interaction between the products of the gene determining neurovirulence and that determining serotype. The nonpathogenic phenotype of a low passage isolate (St. Abb's 84-34 virus), derived from a single tick, generated neurovirulent reassortants. This result indicates that genetic modulation of KEM group viruses may occur in nature.

Deletions of chromosomal regions coding for fimbriae and hemolysins occur in vitro and in vivo in various extra intestinal Escherichia coli isolates

Fimbrial adhesins and hemolysins contribute to pathogenicity of extraintestinal Escherichia coli isolates causing urinary tract infections (UTI), sepsis and new born meningitis (NBM). Using gene cloning techniques and pulse field electrophoresis in combination with Southern hybridizations it was demonstrated that the genetic determinants coding for P and ‘P-related’ fimbrial adhesins and hemolysins are closely linked on the chromosomes of different pathogenic E. coli wild-type isolates. For two UTI strains, 536 (06:K15) and J96 (04:K6), a co-deletion of the linked gene clusters coding for hemolysin and fimbriae was observed. The deleted DNA regions which also comprise flanking DNA sequences were termed ‘pathogenicity DNA islands’. Such ‘pathogenicity DNA islands’ were also detected in the genome of 018:K1 isolates of OMP type 6 but were absent on the chromosomes of O18: K1 strains of OMP type 9. A mutant strain, 536-22 was selected from rat kidneys after intraurethral infection of animals with the wild-type parental strain 536. This particular isolate also shows deletions of ‘pathogenicity islands’ leading to a non-pathogenic phenotype. It is therefore concluded that excisions of ‘pathogenicity islands’ from chromosomes of pathogenic E. coli strains are not restricted to the laboratory but also occur in vivo. The generation of deletions may represent a general mechanism of bacterial virulence modulation.

Effects of a mutation that eliminates UDP glucose-pyrophosphorylase on the pathogenicity of Erwinia carotovora subsp. carotovora.

A nonpathogenic mutant of Erwinia carotovora obtained by Mu d1 mutagenesis was defective in the ability to utilize several carbon sources. The basis of the mutation was analyzed biochemically and shown to be a defect in the ability to form UDP glucose-pyrophosphorylase. The nonpathogenic phenotype of the mutant was caused by its sensitivity to galactose.