https://link.springer.com/content/pdf/10.1186%2Fs40413-015-0073-0.pdf

Meteorological conditions, climate change, new emerging factors, and asthma and related allergic disorders. A statement of the World Allergy Organization

Context 
Studies from different geographical regions have assessed the relations between indoor dampness and mold problems and the risk of asthma, but the evidence has been inconclusive.


Objective 
To assess the relations between indicators of indoor dampness and mold problems and the risk of developing new asthma, and to investigate whether such relations differ according to the type of exposure.


Data sources 
A systematic literature search of PubMed database from 1990 through March 2012 and the reference lists of recent reviews and of relevant articles identified in our search.


Study selection 
Cohort/longitudinal and incident case-control studies assessing the relation between mold/dampness and new asthma were included.


Data extraction 
Three authors independently evaluated eligible articles and extracted relevant information using a structured form.


Synthesis 
Sixteen studies were included: 11 cohort and 5 incident case-control studies. The summary effect estimates (EE) based on the highest and lowest estimates for the relation between any exposure and onset of asthma were 1.50 (95% confidence interval [CI] 1.25–1.80, random-effects model, Q-statistic 38.74 (16), P = 0.001) and 1.31 (95% CI 1.09–1.58, random-effects model, Q-statistic 40.08 (16), P = 0.000), respectively. The summary effect estimates were significantly elevated for dampness (fixed-effects model: EE 1.33, 95% CI 1.12–1.56, Q-statistic 8.22 (9), P = 0.413), visible mold (random-effects model; EE 1.29, 95% CI 1.04–1.60, 30.30 (12), P = 0.001), and mold odor (random-effects model; EE 1.73, 95% CI 1.19–2.50, Q-statistics 14.85 (8), P = 0.038), but not for water damage (fixed-effects model; EE 1.12, 95% CI 0.98–1.27). Heterogeneity was observed in the study-specific effect estimates.


Conclusion 
The evidence indicates that dampness and molds in the home are determinants of developing asthma. The association of the presence of visible mold and especially mold odor to the risk of asthma points towards mold-related causal agents.

/pdf/residential-dampness-and-molds-and-the-risk-of-developing-25a0mo3bga.pdf

Residential Dampness and Molds and the Risk of Developing Asthma: A Systematic Review and Meta-Analysis

Individuals with likely exposure to the highly infectious SARS-CoV-2 do not necessarily develop PCR or antibody positivity, suggesting some may clear sub-clinical infection before seroconversion. T cells can contribute to the rapid clearance of SARS-CoV-2 and other coronavirus infections1-5. We hypothesised that pre-existing memory T cell responses, with cross-protective potential against SARS-CoV-26-12, would expand in vivo to mediate rapid viral control, potentially aborting infection. We studied T cells against the replication transcription complex (RTC) of SARS-CoV-2 since this is transcribed first in the viral life cycle13-15 and should be highly conserved. We measured SARS-CoV-2-reactive T cells in a cohort of intensively monitored healthcare workers (HCW) who remained repeatedly negative by PCR, antibody binding, and neutralisation for SARS-CoV-2 (exposed seronegative, ES). 16-weeks post-recruitment, ES had memory T cells that were stronger and more multispecific than an unexposed pre-pandemic cohort, and more frequently directed against the RTC than the structural protein-dominated responses seen post-detectable infection (matched concurrent cohort). The postulate that HCW with the strongest RTC-specific T cells had an abortive infection was supported by a low-level increase in IFI27 transcript, a robust early innate signature of SARS-CoV-2 infection16. We showed that the RNA-polymerase within RTC was the largest region of high sequence conservation across human seasonal coronaviruses (HCoV) and was preferentially targeted by T cells from UK and Singapore pre-pandemic cohorts and from ES. RTC epitope-specific T cells capable of cross-recognising HCoV variants were identified in ES. Longitudinal samples from ES and an additional validation cohort, showed pre-existing RNA-polymerase-specific T cells expanded in vivo following SARS-CoV-2 exposure, becoming enriched in the memory response of those with abortive compared to overt infection. In summary, we provide evidence of abortive seronegative SARS-CoV-2 infection with expansion of cross-reactive RTC-specific T cells, highlighting these highly conserved proteins as targets for future vaccines against endemic and emerging Coronaviridae.

https://www.medrxiv.org/content/medrxiv/early/2021/07/01/2021.06.26.21259239.full.pdf

Pre-existing polymerase-specific T cells expand in abortive seronegative SARS-CoV-2 infection

Allergy and asthma: Effects of the exposure to particulate matter and biological allergens

HIV is a disease in which the original clinical observations of severe opportunistic infections gave the first clues regarding the underlying pathology, namely that HIV is essentially an infection of the immune system. HIV infects and deletes CD4(+) T cells that normally coordinate the adaptive T- and B-cell response to defend against intracellular pathogens. The immune defect is immediate and profound: At the time of acute infection with an AIDS virus, typically more than half of the gut-associated CD4(+) T cells are depleted, leaving a damaged immune system to contend with a life-long infection.

/pdf/the-t-cell-response-to-hiv-ad1r8pvhtr.pdf

The T-Cell Response to HIV

ObjectivesThe National Asthma Survey—New York State (NYS), a telephone survey of NYS residents, was conducted in 2002–2003 to further understand the burden of asthma among adults and children and 

/pdf/the-national-asthma-survey-new-york-state-association-of-the-2sdjf1toe7.pdf

The National Asthma Survey--New York State: association of the home environment with current asthma status.

HIV-1-specific T lymphocyte responses in individuals exposed to HIV-1 but who remain persistently seronegative (HESNs) have been reported in some but not all previous studies. This study was designed to resolve unequivocally the question of whether HESNs make HIV-1-specific T cell responses. We performed a blind investigation to measure HIV-1-specific T cell responses in both HIV-1-serodiscordant couples and HIV-1-unexposed seronegative controls (HUSNs). We found low-frequency HIV-1-specific T cells in both HESNs and HUSNs but show that the response rates were higher over time in the former (P = 0.01). Furthermore, the magnitudes of the HIV-1-specific T cell responses were significantly higher among responding HESNs than among HUSNs over time (P = 0.002). In both groups, responses were mediated by CD4 T cells. The responses were mapped to single peptides, which often corresponded to epitopes restricted by multiple HLA-DR types that have previously been detected in HIV-1-infected patients. HIV-1-specific T cell responses in HUSNs and some HESNs likely represent cross-reactivity to self or foreign non-HIV-1 antigens. The significantly greater T cell responses in HESNs, including in two who were homozygous for CCR5Δ32, demonstrates that HIV-1-specific T cell responses can be induced or augmented by exposure to HIV-1 without infection.

Differences in HIV-Specific T Cell Responses between HIV-Exposed and -Unexposed HIV-Seronegative Individuals†

We propose methodology for exact statistical tests of hypotheses for models of network dynamics. The methodology formulates Markovian exponential families, then uses sequential importance sampling to compute expectations within basins of attraction and within level sets of a sufficient statistic for an over-dispersion model. Comparisons of hypotheses can be done conditional on basins of attraction. Examples are presented.

/pdf/exact-tests-for-singular-network-data-2bcssu2p6s.pdf

Kruti Pandya

Papers

The National Asthma Survey--New York State: association of the home environment with current asthma status.

Differences in HIV-Specific T Cell Responses between HIV-Exposed and -Unexposed HIV-Seronegative Individuals†

Exact tests for singular network data