Can bacterial interference prevent infection?

The concept that one bacterial species can interfere with the ability of another to colonize and infect the host has at its foundation the prerequisite that bacteria must attach to biological surfaces to cause infection. Although this is an over-simplification of pathogenesis, it has led to studies aimed at creating vaccines that block adhesion events. Arguably, the use of commensal bacteria (also referred to as "normal flora", "indigenous" or "autochthonous" microorganisms) to inhibit pathogens has even greater potential than vaccine use, because these bacteria are natural competitors of pathogens and their action does not require host immune stimulation. Exogenous application of commensal organisms (probiotics) has been shown to reduce the risk of infections in the gut, urogenital tract and wound sites. To manipulate and optimize these effects, further studies are required to understand cell signaling amongst commensals and pathogens within biofilms adherent to host tissues. The potential for new therapeutic regimens using probiotics is significant and worthy of further study.     

Governmental policies on HIV infection in China

This article is a general review of the evolvement of HIV/AIDS-related public policies in China since 1980＇s. It tracks the important laws, regulations and other governmental documents in regard to HIV/AIDS prevention mainly at central level.     

Rule-based simulation of temperate bacteriophage infection: Restriction–modification as a limiter to infection in bacterial populations

An individual-based model (IbM) for bacterial adaptation and evolution, COSMIC-Rules, has been employed to simulate interactions of virtual temperate bacteriophages (phages) and their bacterial hosts. Outcomes of infection mimic those of a phage such as lambda, which can enter either the lytic or lysogenic cycle, depending on the nutritional status of the host. Infection of different hosts possessing differing restriction and modification systems is also simulated. Phages restricted upon infection of one restricting host can be adapted (by host-controlled modification of the phage genome) and subsequently propagate with full efficiency on this host. However, such ability is lost if the progeny phages are passaged through a new host with a different restriction and modification system before attempted re-infection of the original restrictive host. The simulations show that adaptation and re-adaptation to a particular host-controlled restriction and modification system result in lower efficiency and delayed lysis of bacterial cells compared with infection of non-restricting host bacteria.     

Does multiple infection select for raised virulence?

Classical models of virulence evolution conclude that the increased competition favoured by multiple infection will select for increasing consumption and deterioration of the host resource, or 'virulence'. However, recent empirical and theoretical studies suggest that this view of virulence has some shortcomings. Here, we argue that the evolutionary consequences of multiple infection depend critically on whether the exploitation rate of an individual parasite is governed directly by the behaviour of the individual, or whether it is limited by the collective behaviour of the coinfecting group. We illustrate that, depending on the mechanistic details of exploitation, multiple infection can select for reduced virulence.     

Prion infection: Seeded fibrillization or more?

The prion infection is a conversion of host encoded prion protein (PrP) from its cellular isoform PrP^C into the pathological and infectious isoform PrP^Sc; the conversion process was investigated by in vitro studies using recombinant and cellular PrP and natural PrP^Sc. We present a brief summary of the results determined with our in vitro conversion system and the derived mechanistic models. We describe well characterized intermediates and precursor states during the conversion process, kinetic studies of spontaneous and seeded fibrillogenesis and the impact of the membrane environment.Key words: prion protein conversion, seeding, fibril, dimer, precursor state, kinetics, membrane     

Drug-resistant parasites and aggregated infection – early-season dynamics

We investigate the effect of spatial aggregation in the infection dynamics of nematode parasites in ruminants. We show that a high degree of spatial aggregation is likely to lead to a dramatically enhanced rate of invasion by drug-resistant strains. Received: 13 December 1999 / Revised version: 3 April 2000 / Published online: 4 October 2000     

Could a simple surgical intervention eliminate HIV infection?

Background

Human Immunodeficiency Virus (HIV) infection is a dynamic interaction of the pathogen and the host uniquely defined by the preference of the pathogen for a major component of the immune defense of the host. Simple mathematical models of these interactions show that one of the possible outcomes is a chronic infection and much of the modelling work has focused on this state.

Bifurcation

However, the models also predict the existence of a virus-free equilibrium. Which one of the equilibrium states the system selects depends on its parameters. One of these is the net extinction rate of the preferred HIV target, the CD4+ lymphocyte. The theory predicts, somewhat counterintuitively, that above a critical extinction rate, the host could eliminate the virus. The question then is how to increase the extinction rate of lymphocytes over a period of several weeks to several months without affecting other parameters of the system.

Testing the hypothesis

Proposed here is the use of drainage, or filtration, of the thoracic duct lymph, a well-established surgical technique developed as an alternative for drug immunosuppression for organ transplantation. The performance of clinically tested thoracic duct lymphocyte depletion schemes matches theoretically predicted requirements for HIV elimination.

     

Quantitative analysis of the bacteriophage Qβ infection cycle

In this study, the infection cycle of bacteriophage Qβ was investigated. Adsorption of bacteriophage Qβ to Escherichia coli is explained in terms of a collision reaction, the rate constant of which was estimated to be 4 × 10^− 10 ml/cells/min. In infected cells, approximately 130 molecules of β-subunit and 2 × 10⁵ molecules of coat protein were translated in 15 min. Replication of Qβ RNA proceeded in 2 steps—an exponential phase until 20 min and a non-exponential phase after 30 min. Prior to the burst of infected cells, phage RNAs and coat proteins accumulated in the cells at an average of up to 2300 molecules and 5 × 10⁵ molecules, respectively. An average of 90 infectious phage particles per infected cell was released during a single infection cycle up to 105 min.     

Is persistent bacterial infection good for your health?

Certain bacterial pathogens have evolved to survive in their human hosts for long periods without causing harm. Is it possible that these persistent bacterial infections provide a protective benefit to the host?     

How often is genital yeast infection sexually transmitted?

We analysed data from a computer-based bank of clinical records of patients seen in a clinic for sexually transmitted diseases over a three-year period to investigate the association between genital yeast infections and sexually transmitted diseases (STDs). We classified STDs as primary and secondary syphilis; gonorrhoea; lymphogranuloma venereum; trichomoniasis; scabies; pediculosis; genital herpes; warts; and molluscum contagiosum. Of a total of 2984 disease episodes among women, 1054 (35-3%) included yeast infections, whereas only 382 (6-9%) of 5501 episodes in heterosexual men were associated with yeast infections, We found a significant association between yeast infection and STD and non-specific genital infection (non-specific urethritis (NSU) and procitis in men, and female contacts of men with NSU), which suggested that yeast infection was sexually acquired in 414 out of 1054 disease episodes in women (39%) and 110 out of 382 episodes in heterosexual men (29%). We conclude that sexually active patients with genital yeast infections should be screened for other STDs particularly non-specific genital infection.