In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Background: The novel corona virus SARS-CoV-2 (COVID-19) can infect healthcare workers. We developed an institutional algorithm to protect operating room team members during the COVID-19 pandemic and rationally conserve personal protective equipment (PPE). Study Design: An interventional platform (operating room, interventional suites, and endoscopy) PPE taskforce was convened by the hospital and medical school leadership and tasked with developing a common algorithm for PPE use, to be used throughout the interventional platform. In conjunction with our infection disease experts, we developed our guidelines based upon potential patterns of spread, risk of exposure and conservation of PPE. A decision tree algorithm describing our institutional guidelines for precautions for operating room team members was created. This algorithm is based on urgency of operation, anticipated viral burden at the surgical site, opportunity for a procedure to aerosolize virus, and likelihood a patient could be infected based on symptoms and testing. Conclusion: Despite COVID-19 being a new threat, we have shown that by developing an easyto-follow decision tree algorithm for the interventional platform teams, we can ensure optimal healthcare worker safety.
Journal Pre-proof Precautions for Operating Room Team Members during the COVID-19 Pandemic Precautions for Operating Room Team Members during the COVID-19 Pandemic

The recent outbreak of the human Zaire ebolavirus (EBOV) epidemic is spiraling out of control in West Africa. Human EBOV hemorrhagic fever has a case fatality rate of up to 90%. The EBOV is classified as a biosafety level 4 pathogen and is considered a category A agent of bioterrorism by Centers for Disease Control and Prevention, with no approved therapies and vaccines available for its treatment apart from supportive care. Although several promising therapeutic agents and vaccines against EBOV are undergoing the Phase I human trial, the current epidemic might be outpacing the speed at which drugs and vaccines can be produced. Like all viruses, the EBOV largely relies on host cell factors and physiological processes for its entry, replication, and egress. We have reviewed currently available therapeutic agents that have been shown to be effective in suppressing the proliferation of the EBOV in cell cultures or animal studies. Most of the therapeutic agents in this review are directed against non-mutable targets of the host, which is independent of viral mutation. These medications are approved by the Food and Drug Administration (FDA) for the treatment of other diseases. They are available and stockpileable for immediate use. They may also have a complementary role to those therapeutic agents under development that are directed against the mutable targets of the EBOV.
Human Ebola virus infection in West Africa: a review of available therapeutic agents that target different steps of the life cycle of Ebola virus-mutable host cell therapeutic targets for Ebola virus, Cocktail therapeutic intervention for RNA virus Multilingual abstract

Leishmaniasis is a parasitic disease that courses with cutaneous or visceral clinical manifestations. The amastigote stage of the parasite infects phagocytes and modulates the effector function of the host cells. Our group has described that the interaction between Leishmania and immature monocyte-derived dendritic cells (DCs) takes place through dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), a C-type lectin that specifically recognizes fungal, viral and bacterial pathogens. The DC-SIGN-mediated recognition of Leishmania amastigotes does not induce DC maturation, and the DC-SIGN ligand/s on Leishmania parasites is/are still unknown. We have also found that the DC-SIGN-related molecule L-SIGN, specifically expressed in lymph node and liver sinusoidal endothelial cells, acts as a receptor for L. infantum, the parasite responsible for visceral leishmaniasis, but does not recognize L. pifanoi, which causes the cutaneous form of the disease. Therefore, DC-SIGN and L-SIGN differ in their ability to interact with Leishmania species responsible for either visceral or cutaneous leishmaniasis. A deeper knowledge of the parasite-Ctype lectin interaction may be helpful for the design of new DC-based therapeutic vaccines against Leishmania infections.

Role of the C-type lectins DC-SIGN and L-SIGN in Leishmania interaction with host phagocytes