No abstract

evere infection with COVID-19 has been linked to immune dysregulation, including impaired or delayed production of type I and type III interferons 1-5 , marked lymphopenia [6][7][8][9][10] and a paradoxical increase in pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 1,4,6,[11][12][13] . Alteration of T cell compartments include increases in effector and activated CD4 and CD8 T cells [14][15][16][17] , CD8 + T cells contribute to survival in patients with COVID-19 and hematologic cancer

Based on the known and emerging biology of autoimmune diseases and COVID‐19, it was hypothesised that whilst B‐cell depletion should not necessarily expose people to severe SARS‐CoV‐2‐related issues, it may inhibit or blunt the protective immunity following infection and vaccination. This is supported clinically, as the majority of SARS‐CoV‐2 infected, CD20‐depleted people with autoimmunity, have recovered. However, in CD‐20 treated people until naïve B‐cells repopulate, based on B‐cell repopulation‐kinetics and vaccination responses, from published rituximab, and unpublished ocrelizumab (NCT00676715, NCT02545868) trial data shown here suggests that it may be possible to undertake dose‐interruption to maintain inflammatory disease control, whilst allowing effective vaccination against SARS‐CoV‐29, if and when an effective vaccine is available.

The aim of this paper is to consider the diagnostic criteria for tuberculosis in ancient populations. It investigates the frequency of periosteal new bone formation on the visceral surfaces of ribs from 1718 individuals from the Terry Collection, Smithsonian Institution, Washington D.C. and attempts to determine the aetiological factors producing these lesions. Numbers of individuals with lesions according to cause of death were recorded and the patterning of lesions compared between people who had died from tuberculosis and those whose cause of death was unrelated to a pulmonary disease. Rib lesions were more common in individuals dying from tuberculosis (61.6% or 157 of 255) than in individuals dying from other causes (15.2% or 165 of 1086). It is suggested that tuberculosis at a peripheral lung focus may disseminate directly through the pleura to the visceral surfaces of the ribs, or that pulmonary tuberculosis may be the cause of empyema of the pleural cavity and that this, per se, may initiate inflammatory change on the visceral surfaces of ribs. The nonrecognition or description of these often very subtle proliferative lesions on ribs by radiological examination of tuberculous victims is significant in the discussion of bone changes in tuberculosis. The possibility that individuals with no recorded history of tuberculosis at death actually suffered from the disease was considered in light of the frequency of rib lesions and noncorrelation with a tuberculous cause of death. Differential diagnoses are discussed including the possibility that the lesions represent a general non-specific indicator of stress.

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