The Wood equation allows consistent fitting of individual antibody-response profiles of Zika virus or SARS-CoV-2 infected patients.

Antibody kinetic curves obtained during a viral infection are often fitted using aggregated patient data, hiding the heterogeneity of individual humoral immune responses. Individual antibody responses can be modeled using the Wood equation and grouped according to their profile. Such modeling takes into account several important kinetic parameters, such as the day when antibody detection becomes positive [daypos], the day of the maximal response [daymax], the maximum antibody level [levelmax], and the day when antibody detection becomes negative [dayneg]. Potential associations between these profiles and studied factors can then be tested.

Placental malaria, maternal HIV infection and infant morbidity.

Co-infection with malaria and HIV in pregnant women is particularly common in sub-Saharan Africa and has serious consequences for both mother and newborn child. Numerous studies have been published on the effects in pregnancy of HIV on malaria infection and on the effects of malaria on HIV infection. The increased prevalence and intensity of parasitaemia (placental and peripheral infection and parasite density) in HIV-infected women is well established. Similarly, malaria infection seems to be associated with higher viral loads. However, there is still uncertainty as to the influence of malaria on the clinical course of HIV infection, mother-to-child transmission of HIV, and the consequences of co-infection on post-neonatal infant morbidity and mortality. These questions require further investigation. In terms of prevention, intermittent preventive treatment with two doses of sulfadoxine-pyrimethamine (SP) has been found less effective in preventing malaria in HIV-infected than uninfected women, and a higher dosage (such as monthly SP) has been recommended. Regarding malaria, there is also a lack of clear recommendations for women taking daily cotrimoxazole prophylaxis, and anti-malarial-anti-retroviral interactions are not well understood. Multi-centre clinical trials should be undertaken to investigate effective, coherent and well-tolerated strategies to prevent malaria in HIV-infected women. Safe alternatives to SP should be identified and evaluated rapidly. Finally, a central pharmaco-vigilance network should be instituted to report adverse effects.

Expression of the endogenous type II secretion pathway in Escherichia coli leads to chitinase secretion.

Escherichia coli K-12, the most widely used laboratory bacterium, does not secrete proteins into the extracellular medium under standard growth conditions, despite possessing chromosomal genes encoding a putative type II secretion machinery (secreton). We show that in wild-type E.coli K-12, divergent transcription of the two operons in the main chromosomal gsp locus, encoding the majority of the secreton components, is silenced by the nucleoid-structuring protein H-NS. In mutants lacking H-NS, the secreton genes cloned on a moderate-copy-number plasmid are expressed and promote efficient secretion of the endogenous, co-regulated endochitinase ChiA. This is the first time that secretion of an endogenous extracellular protein has been demonstrated in E.coli K-12.

The ChiA (YheB) protein of Escherichia coli K-12 is an endochitinase whose gene is negatively controlled by the nucleoid-structuring protein H-NS.

The chromosome of Escherichia coli K-12 contains a putative gene, yheB (chiA), at centisome 74.7, whose product shows sequence similarity with chitinases of bacterial and viral origin. We cloned the chiA (yheB) gene and demonstrated that it codes for a 94.5 kDa periplasmic protein with endochitinase/lysozyme activity. Under standard laboratory growth conditions, chiA expression is very low, as shown by the Lac- phenotype of a chiA transcriptional fusion to a promoterless lacZ reporter. To identify factors that control chitinase gene expression, we generated random Tn10 insertions in the chromosome of the fusion-containing strain, selecting for a Lac+ phenotype. The majority of the mutations that caused a Lac+ phenotype mapped to the hns gene, encoding the nucleoid-structuring protein H-NS. Transcription of chiA in vivo is driven by a single sigma70 promoter and is derepressed in an hns mutant. Using a competitive gel retardation assay, we demonstrated that H-NS binds directly and with high affinity to the chiA promoter region. In addition to hns, other E. coli mutations causing defects in global regulatory proteins, such as fis, crp or stpA in combination with hns, increased chiA expression to different extents, as did decreasing the growth temperature from 37 degrees C to 30 degrees C. A possible physiological function of ChiA (YheB) endochitinase in E. coli K-12 is discussed.

Isolation and characterization of vicH, encoding a new pleiotropic regulator in Vibrio cholerae.

During the last decade, the hns gene and its product, the H-NS protein, have been extensively studied in Escherichia coli. H-NS-like proteins seem to be widespread in gram-negative bacteria. However, unlike in E. coli and in Salmonella enterica serovar Typhimurium, little is known about their role in the physiology of those organisms. In this report, we describe the isolation of vicH, an hns-like gene in Vibrio cholerae, the etiological agent of cholera. This gene was isolated from a V. cholerae genomic library by complementation of different phenotypes associated with an hns mutation in E. coli. It encodes a 135-amino-acid protein showing approximately 50% identity with both H-NS and StpA in E. coli. Despite a low amino acid conservation in the N-terminal part, VicH is able to cross-react with anti-H-NS antibodies and to form oligomers in vitro. The vicH gene is expressed as a single gene from two promoters in tandem and is induced by cold shock. A V. cholerae wild-type strain expressing a vicHDelta92 gene lacking its 3' end shows pleiotropic alterations with regard to mucoidy and salicin metabolism. Moreover, this strain is unable to swarm on semisolid medium. Similarly, overexpression of the vicH wild-type gene results in an alteration of swarming behavior. This suggests that VicH could be involved in the virulence process in V. cholerae, in particular by affecting flagellum biosynthesis.