SARS-CoV-2 delta AY.1 variant cluster in an accommodation facility for COVID-19: Research study

Background This is a case report on a cluster infection of novel severe acute respiratory syndrome coronavirus 2 delta AY.1 variant at an accommodation facility and the subsequent attempts to isolate individuals who tested positive. Methods The background that facilitated this cluster was investigated, and the conditions in which infection was established, the infection route, and the effectiveness of routine measures were evaluated. Ninety-nine staff members had been working at the accommodation facility at the time of infection, and it was estimated that 10 members were infected with the delta AY.1 variant. Results Our results suggest that infection of staff from a patient staying overnight should be excluded. The factors contributing to the cluster infection involved short-distance conversations with individuals wearing non-woven three-layer masks moved out of position (non-woven) and gathering together with individuals wearing non-woven masks in hypoventilated conditions. Our findings also indicate that this variant is possibly airborne and can infect individuals in enclosed spaces with poor ventilation, even when either infected or exposed individuals wear non-woven masks. Conclusions The routine maintenance of systems established for the detection of infections and prompt and appropriate preventive measures following the identification of positive individuals will help prevent further cluster infections.

SARS-CoV-2 Delta AY.1 variant Cluster in an accommodation facility for COVID-19

This is a case report on a cluster infection of novel severe acute respiratory syndrome coronavirus 2 delta AY.1 variant at an accommodation facility and the subsequent attempts to isolate individuals who tested positive. The background that facilitated this cluster was investigated, and the conditions in which infection was established, the infection route, and the effectiveness of routine measures were evaluated. Ninety-nine staff members had been working at the accommodation facility at the time of infection, and it was estimated that 10 members were infected with the delta AY.1 variant. Our results suggest that infection of staff from a patient staying overnight should be excluded. The factors contributing to the cluster infection involved short-distance conversations with individuals wearing non-woven three-layer masks moved out of position (non-woven) and gathering together with individuals wearing non-woven masks in hypoventilated conditions. Our findings also indicate that this variant is possibly airborne and can infect individuals in enclosed spaces with poor ventilation, even when either infected or exposed individuals wear non-woven masks. The routine maintenance of systems established for the detection of infections and prompt and appropriate preventive measures following the identification of positive individuals will help prevent further cluster infections.

A bivalent vaccine of Eimeria media and Eimeria intestinalis yields protective immunity against coccidiosis during rabbit production

Coccidiosis is the costliest disease in the rabbit industry. The kits do not obtain maternal immunity against the diseases and therefore suckling to weaning period being the riskiest time of infection. To date, control of coccidiosis is relied on the use of chemical coccidiostat as a drug or as the substance in feed. Whilst, continuous exposure to antibiotics develops resistance and contamination in the carcass. There is no commercially provided vaccine to prevent rabbit coccidiosis cases. In this report, we processed precocious lines from the strain of Yogyakarta origin by using selection pressure to attenuate Eimeria spp. The vaccine candidate composed of 50% of each Eimeria media and Eimeria intestinalis were given orally to initiate protective immunity against rabbit coccidiosis. The vaccinated groups with 5 x 102 oocyst dosage exhibited 95% less total oocyst excretion compared to the non-vaccinated group. Our experiment showed no mortality and without any significantly detrimental response of vaccinated rabbits during the observation time (P<0.0001). Since the oocysts in the vaccinated rabbits are excreted in dropped faecal samples, it provides recirculation and provokes a group immunity within the flock. A vaccine candidate is a promising tool as a more environmentally friendly strategy for sustainable rabbit production.

Infection, inflammation and thrombosis: a review of potential mechanisms mediating arterial thrombosis associated with influenza and severe acute respiratory syndrome coronavirus 2

Thrombosis has long been reported as a potentially deadly complication of respiratory viral infections and has recently received much attention during the global coronavirus disease 2019 pandemic. Increased risk of myocardial infarction has been reported during active infections with respiratory viruses, including influenza and severe acute respiratory syndrome coronavirus 2, which persists even after the virus has cleared. These clinical observations suggest an ongoing interaction between these respiratory viruses with the host’s coagulation and immune systems that is initiated at the time of infection but may continue long after the virus has been cleared. In this review, we discuss the epidemiology of viral-associated myocardial infarction, highlight recent clinical studies supporting a causal connection, and detail how the virus’ interaction with the host’s coagulation and immune systems can potentially mediate arterial thrombosis.

Respiratory Viruses Among Ethnic Nicobarese During COVID-19 Pandemic

Background: Acute respiratory infections (ARIs) and severe acute respiratory illness (SARI) are public health burdens globally. The percentage of non-SARS CoV-2 respiratory viruses among patients having ARI and SARI who visit Car Nicobar's hospital settings is undocumented. Changes in the epidemiology of other respiratory viruses during COVID19 pandemic is being reported worldwide.Methods: Inpatient and outpatient settings at BJR hospital, Car Nicobar Island, India, were used to conduct prospective monitoring for ARI and SARI among Nicobarese tribal members. The patients with ARI and SARI were enlisted in BJR hospital from June 2019 to May 2021. At the ICMR-NIV in Pune, duplex qRTPCR assays were used to test the presence of respiratory viruses. The prevalence of non- SARS CoV-2 respiratory viruses was measured by comparing here between pandemic and pre-pandemic periods.Results: During the COVID19 pandemic, Influenza A (H3N2) (55.7%), and rhinovirus (12.5%) were predominantly reported non-SARS CoV-2 respiratory viruses while Human metapneumovirus (48.1%) and influenza A (H1N1)pdm09 (18.5%) were most commonly reported in the prepandemic period. This result indicates the altered circulation of non-SARS CoV-2 during pandemic.Conclusions: A considerable proportion of respiratory infection was correlated with respiratory viruses. Prevalence of non-SARS CoV-2 respiratory viruses was high at the time of infection when compared with pre-pandemic period, at Car Nicobar Island. This study enlightened the change in circulation of other respiratory viruses among the indigenous Nicobarese tribes. Clinicians and allied medical staff should be more prudent of these respiratory infections.

The effect of new Mycobacterium tuberculosis infection on the sensitivity of prognostic TB signatures

BACKGROUND: Tests that identify individuals at greatest risk of TB will allow more efficient targeting of preventive therapy. The WHO target product profile for such tests defines optimal sensitivity of 90% and minimum sensitivity of 75% for predicting incident TB. The CORTIS (Correlate of Risk Targeted Intervention Study) evaluated a blood transcriptomic signature (RISK11) for predicting incident TB in a high transmission setting. RISK11 is able to predict TB disease progression but optimal prognostic performance was limited to a 6-month horizon.METHODS: Using a mathematical model, we estimated how subsequent Mycobacterium tuberculosis (MTB) infection may have contributed to the decline in sensitivity of RISK11. We calculated the effect at different RISK11 thresholds (60% and 26%) and for different assumptions about the risk of MTB infection.RESULTS: Modelled sensitivity over 15 months, excluding new infection, was 28.7% (95% CI 12.3–74.1) compared to 25.0% (95% CI 12.7–45.9) observed in the trial. Modelled sensitivity exceeded the minimum criteria (>75%) over a 9-month horizon at the 60% threshold and over 12 months at the 26% threshold.CONCLUSIONS: The effect of new infection on prognostic signature performance is likely to be small. Signatures such as RISK11 may be most useful in individuals, such as household contacts, where probable time of infection is known.

Immunity and Protection – Basic Considerations

Innate and adaptive immunity generate pathogen-specific antibodies and cells as basis for the efficacy and effectiveness of vaccines: immunity results in protection. For almost all currently licensed vaccines, functional antibodies are the most relevant mechanism of action; they work by binding of an antigen, agglutination, neutralization, complement activation and opsonization directed against specific pathogens or toxins. Immune memory generated by either infection or vaccine priming allows rapid production of antibodies and immune cells (3-7 days) upon later re-infection or (booster-) vaccination. Vaccine-induced immunity may result in protection even in the absence of any measurable specific antibodies at the time of infection – due to memory cells, and due to the effects of T-cells. CD4+ T-cells (“T-helper cells”) induce protection largely by cytokine production, CD8+ T-cells can directly or indirectly kill infected or cancerous cells and they can help clear infections. While antibodies against vaccine antigens can easily be measured by a variety of methods, testing for specific T-cell immunity is less well standardized and more difficult to perform. The term “seroprotection” indicates a serological value (e.g. a titre), associated with protection used for the purpose of vaccine licensure. Measurements of seroprotection can be the percentage of seroresponders, GMTs, fold rise of antibodies or RCD curves. In real life, many factors may contribute to individual protection in both, a positive and a negative direction, including factors inherent with the infecting pathogen, epidemiological factors, host factors, and characteristics of the vaccine and vaccination. Unlike general public belief, the “failure to vaccinate” is more relevant than “vaccine failures” in a population.

Characterization of pathogenic CD8 + T cells in Chlamydia - infected OT1 mice

Chlamydia trachomatis is a leading infectious cause of infertility in women due to its induction of lasting pathology such as hydrosalpinx. Chlamydia muridarum induces mouse hydrosalpinx because C. muridarum can both invade tubal epithelia directly (as a 1 st hit) and induce lymphocytes to promote hydrosalpinx indirectly (as a 2 nd hit). In the current study, a critical role of CD8 + T cells in chlamydial induction of hydrosalpinx was validated in both wild type C57BL/6J and OT1 transgenic mice. OT1 mice failed to develop hydrosalpinx partially due to the failure of their lymphocytes to recognize chlamydial antigens. CD8 + T cells from naïve C57BL/6J rescued the recipient OT1 mice to develop hydrosalpinx when naïve CD8 + T cells were transferred at the time of infection with Chlamydia . However, when the transfer was delayed for 2 weeks or longer after the chlamydial infection, naïve CD8 + T cells no longer promoted hydrosalpinx. Nevertheless, Chlamydia -immunized CD8 + T cells still promoted significant hydrosalpinx in the recipient OT1 mice even when the transfer was delayed for 3 weeks. Thus, CD8 + T cells must be primed within 2 weeks after chlamydial infection to be pathogenic but once primed, they can promote hydrosalpinx for >3 weeks. However, Chlamydia -primed CD4 + T cells failed to promote chlamydial induction of pathology in OT1 mice. This study has optimized an OT1 mouse-based model for revealing the pathogenic mechanisms of Chlamydia -specific CD8 + T cells.