Association between different anti-Tat antibody isotypes and HIV disease progression: data from an African cohort

Background: The presence of IgG and IgM against Tat, an HIV protein important for viral replication and immune dysfunction, is associated with slow disease progression in clade B HIV-infected individuals. However, although Tat activities strictly depend on the viral clade, our knowledge about the importance of anti-Tat antibodies in non-clade B HIV infection is poor. The objective of this study was to investigate the association of different anti-Tat antibody isotypes with disease progression in non-clade B HIV-infected subjects and to study the relationship between anti-Tat humoral responses and immunological abnormalities. Methods: Anti-clade B and - clade C Tat IgG, IgM and IgA titers were assessed in serum samples from 96 cART-naive subjects with chronic HIV infection from Mbeya, Tanzania, and associated with CD4(+) T cell count, plasma viremia and CD4(+) and CD8(+) T cell phenotypes. Results: Anti-Tat IgM were preferentially detected in chronic HIV-infected subjects with low T cell activation (p-value = 0.03) and correlated with higher CD4(+) T cell counts and lower viral loads irrespective of the duration of infection (p-value = 0.019 and p-value = 0.037 respectively). Conversely, anti-Tat IgA were preferentially detected in individuals with low CD4(+) T cell counts and high viral load (p-value = 0.02 and p-value < 0.001 respectively). The simultaneous presence of anti-Tat IgG and IgM protected from fast CD4(+) T cell decline (p-value < 0.01) and accumulation of CD38(+) HLADR(+) CD8(+) T cells (p-value = 0.029). Conclusions: Anti-Tat IgG alone are not protective in non-clade B infected subjects, unless concomitant with IgM, suggesting a protective role of persistent anti-Tat IgM irrespective of the infecting clade

Impact of the COVID-19 pandemic on patients with paediatric cancer in low-income, middle-income and high-income countries: a multicentre, international, observational cohort study

OBJECTIVES: Paediatric cancer is a leading cause of death for children. Children in low-income and middle-income countries (LMICs) were four times more likely to die than children in high-income countries (HICs). This study aimed to test the hypothesis that the COVID-19 pandemic had affected the delivery of healthcare services worldwide, and exacerbated the disparity in paediatric cancer outcomes between LMICs and HICs. DESIGN: A multicentre, international, collaborative cohort study. SETTING: 91 hospitals and cancer centres in 39 countries providing cancer treatment to paediatric patients between March and December 2020. PARTICIPANTS: Patients were included if they were under the age of 18 years, and newly diagnosed with or undergoing active cancer treatment for Acute lymphoblastic leukaemia, non-Hodgkin's lymphoma, Hodgkin lymphoma, Wilms' tumour, sarcoma, retinoblastoma, gliomas, medulloblastomas or neuroblastomas, in keeping with the WHO Global Initiative for Childhood Cancer. MAIN OUTCOME MEASURE: All-cause mortality at 30 days and 90 days. RESULTS: 1660 patients were recruited. 219 children had changes to their treatment due to the pandemic. Patients in LMICs were primarily affected (n=182/219, 83.1%). Relative to patients with paediatric cancer in HICs, patients with paediatric cancer in LMICs had 12.1 (95% CI 2.93 to 50.3) and 7.9 (95% CI 3.2 to 19.7) times the odds of death at 30 days and 90 days, respectively, after presentation during the COVID-19 pandemic (p<0.001). After adjusting for confounders, patients with paediatric cancer in LMICs had 15.6 (95% CI 3.7 to 65.8) times the odds of death at 30 days (p<0.001). CONCLUSIONS: The COVID-19 pandemic has affected paediatric oncology service provision. It has disproportionately affected patients in LMICs, highlighting and compounding existing disparities in healthcare systems globally that need addressing urgently. However, many patients with paediatric cancer continued to receive their normal standard of care. This speaks to the adaptability and resilience of healthcare systems and healthcare workers globally

Twelve-month observational study of children with cancer in 41 countries during the COVID-19 pandemic

Childhood cancer is a leading cause of death. It is unclear whether the COVID-19 pandemic has impacted childhood cancer mortality. In this study, we aimed to establish all-cause mortality rates for childhood cancers during the COVID-19 pandemic and determine the factors associated with mortality

Search for the rare hadronic decay Bs0→ppˉB_s^0\to p \bar{p}

A search for the rare hadronic decay Bs0→pp¯ is performed using proton-proton collision data recorded by the LHCb experiment at a center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 6  fb-1. No evidence of the decay is found and an upper limit on its branching fraction is set at B(Bs0→pp¯)&lt;4.4(5.1)×10-9 at 90% (95%) confidence level; this is currently the world’s best upper limit. The decay mode B0→pp¯ is measured with very large significance, confirming the first observation by the LHCb experiment in 2017. The branching fraction is determined to be B(B0→pp¯)=(1.27±0.15±0.05±0.04)×10-8, where the first uncertainty is statistical, the second is systematic and the third is due to the external branching fraction of the normalization channel B0→K+π-. The combination of the two LHCb measurements of the B0→pp¯ branching fraction yields B(B0→pp¯)=(1.27±0.13±0.05±0.03)×10-8.A search for the rare hadronic decay $B_s^0\to p \bar{p}$ is performed using proton-proton collision data recorded by the LHCb experiment at a center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 6 fb$^{-1}$. No evidence of the decay is found and an upper limit on its branching fraction is set at ${\cal B}(B_s^0\to p \bar{p}) < 4.4~(5.1) \times 10^{-9}$ at 90% (95%) confidence level; this is currently the world's best upper limit. The decay mode $B^0\to p \bar{p}$ is measured with very large significance, confirming the first observation by the LHCb experiment in 2017. The branching fraction is determined to be ${\cal B}(B^0\to p \bar{p}) = \rm (1.27 \pm 0.15 \pm 0.05 \pm 0.04) \times 10^{-8}$, where the first uncertainty is statistical, the second is systematic and the third is due to the external branching fraction of the normalization channel $B^0\to K^+\pi^-$. The combination of the two LHCb measurements of the $B^0\to p \bar{p}$ branching fraction yields ${\cal B}(B^0\to p \bar{p}) = \rm (1.27 \pm 0.13 \pm 0.05 \pm 0.03) \times 10^{-8}$

Observation of sizeable ω\omega contribution to χc1(3872)→π+π−J/ψ\chi_{c1}(3872) \to \pi^+\pi^- J/\psi decays

Resonant structures in the dipion mass spectrum from $\chi_{c1}(3872)\to\pi^+\pi^- J/\psi$ decays, produced via $B^+\to K^+\chi_{c1}(3872)$ decays, are analyzed using proton-proton collision data collected by the LHCb experiment, corresponding to an integrated luminosity of 9 fb$^{-1}$. A sizeable contribution from the isospin conserving $\chi_{c1}(3872)\to\omega J/\psi$ decay is established for the first time, $(21.4\pm2.3\pm2.0)\%$, with a significance of more than $7.1\sigma$. The amplitude of isospin violating decay, $\chi_{c1}(3872)\to\rho^0 J/\psi$, relative to isospin conserving decay, $\chi_{c1}(3872)\to\omega J/\psi$, is properly determined, and it is a factor of six larger than expected for a pure charmonium state.Resonant structures in the dipion mass spectrum from χc1(3872)→π+π-J/ψ decays, produced via B+→K+χc1(3872) decays, are analyzed using proton-proton collision data collected by the LHCb experiment, corresponding to an integrated luminosity of 9  fb-1. A sizeable contribution from the isospin conserving χc1(3872)→ωJ/ψ decay is established for the first time, (21.4±2.3±2.0)%, with a significance of more than 7.1σ. The amplitude of isospin violating decay, χc1(3872)→ρ0J/ψ, relative to isospin conserving decay, χc1(3872)→ωJ/ψ, is properly determined, and it is a factor of 6 larger than expected for a pure charmonium state.Resonant structures in the dipion mass spectrum from $\chi_{c1}(3872)\to\pi^+\pi^- J/\psi$ decays, produced via $B^+\to K^+\chi_{c1}(3872)$ decays, are analyzed using proton-proton collision data collected by the LHCb experiment, corresponding to an integrated luminosity of 9 $fb^{-1}$. A sizeable contribution from the isospin conserving $\chi_{c1}(3872)\to\omega J/\psi$ decay is established for the first time, $(21.4\pm2.3\pm2.0)\%$, with a significance of more than $7.1\sigma$. The amplitude of isospin violating decay, $\chi_{c1}(3872)\to\rho^0 J/\psi$, relative to isospin conserving decay, $\chi_{c1}(3872)\to\omega J/\psi$, is properly determined, and it is a factor of six larger than expected for a pure charmonium state