Heat sterilisation dramatically reduces filter efficiency of the majority of FFP2 and KN-95 respirators.

BACKGROUND: Because of the enormous demand for personal protective equipment and especially respiratory protective devices (respirators) during the initial phase of the corona pandemic shortages arose. Sterilisation of used respirators can reduce these shortages. In our study, respirator testing was carried out after only one sterilisation cycle. AIM: To determine if steam sterilisation and reuse could be safely applied for used respirators. METHODS: In a cabinet an aqueous solution of NaCl (0.02% w/v) was nebulized and passed through a sample of the material of a respirator. Passing particle concentrations were measured directly from the cabinet and via the filter material of the respirator for particles ≥ 0.3 µm, ≥ 0.5 µm and ≥ 1.0 µm. FINDINGS: only three out of ten steam sterilised respirators met the requirements of 94% filtration efficiency. CONCLUSION: The results prove that heat sterilisation cannot be generically applied for reuse of respirators safely.

The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin-angiotensin system.

The SARS-CoV-2 pandemic is a healthcare crisis caused by insufficient knowledge applicable to effectively combat the virus. Therefore, different scientific discovery strategies need to be connected, to generate a rational treatment which can be made available as rapidly as possible. This relies on a solid theoretical understanding of the mechanisms of SARS-CoV-2 infection and host responses, which is coupled to the practical experience of clinicians that are treating patients. Because SARS-CoV-2 enters the cell by binding to angiotensin-converting enzyme 2 (ACE2), targeting ACE2 to prevent such binding seems an obvious strategy to combat infection. However, ACE2 performs its functions outside the cell and was found to enter the cell only by angiotensin II type 1 receptor (AT1R)-induced endocytosis, after which ACE2 is destroyed. This means that preventing uptake of ACE2 into the cell by blocking AT1R would be a more logical approach to limit entry of SARS-CoV-2 into the cell. Since ACE2 plays an important protective role in maintaining key biological processes, treatments should not disrupt the functional capacity of ACE2, to counterbalance the negative effects of the infection. Based on known mechanisms and knowledge of the characteristics of SARS-CoV we propose the hypothesis that the immune system facilitates SARS-CoV-2 replication which disrupts immune regulatory mechanisms. The proposed mechanism by which SARS-CoV-2 causes disease immediately suggests a possible treatment, since the AT1R is a key player in this whole process. AT1R antagonists appear to be the ideal candidate for the treatment of SARS-CoV-2 infection. AT1R antagonists counterbalance the negative consequences of angiotesnin II and, in addition, they might even be involved in preventing the cellular uptake of the virus without interfering with ACE2 function. AT1R antagonists are widely available, cheap, and safe. Therefore, we propose to consider using AT1R antagonists in the treatment of SARS-CoV-2.