COVID-19 Patientinnen und Patienten haben ein hohes thrombotisches Risiko. Die Sicherheit und Wirksamkeit verschiedener Antikoagulationsschemata bei COVID-19 Patientinnen und Patienten sind unklar. Acht RCTs mit 5580 Patientinnen und Patienten wurden identifiziert, wovon zwei RCTs Antikoagulation in halbtherapeutischer und sechs RCTs Antikoagulation in therapeutischer Dosierung mit der Standard Thromboembolieprophylaxe verglichen haben. Die halbtherapeutische Antikoagulation kann wenig oder gar keinen Einfluss auf thrombotische Ereignisse oder Todesfälle haben (RR 1,03, 95% KI 0,86-1,24), kann aber schwere Blutungen (RR 1,48, 95% KI 0,53-4,15) bei mittelschweren bis schweren COVID-19 Patientinnen und Patienten verstärken. Therapeutische Antikoagulation kann thrombotische Ereignisse oder den Tod bei Patientinnen und Patienten mit mittelschwerem COVID-19 (RR 0,64, 95% KI 0,38-1,07) verringern, kann aber bei Patientinnen und Patienten mit schwerer Erkrankung (RR 0,98, 95% KI 0,86-1,12) wenig oder keine Wirkung haben. Das Risiko schwerer Blutungen kann unabhängig vom Schweregrad der Erkrankung zunehmen (RR 1,78, 95% KI 1,15-2,74). Die Evidenzsicherheit ist immer noch gering. Mäßig betroffene COVID-19 Patientinnen und Patienten können von einer therapeutischen Antikoagulation profitieren, jedoch ist das Blutungsrisiko erhöht. / COVID-19 patients have a high risk of thrombotic disease. The safety and efficacy of various anticoagulation regimens in COVID-19 patients remains unclear. Eight RCTs with 5580 patients were identified, with two comparing anticoagulation in intermediate doses and six comparing therapeutic doses to standard thromboembolism prophylaxis. Intermediate anticoagulation may have little or no effect on thrombotic events or deaths (RR 1.03, 95% CI 0.86-1.24), but may increase major bleeding (RR 1.48, 95% CI 0.53-4.15) in moderate to severe COVID-19 patients. Therapeutic anticoagulation may reduce thrombotic events or death in patients with moderate COVID-19 (RR 0.64, 95% CI 0.38-1.07), but may have little or no effect in patients with severe disease (RR 0.98, 95% CI 0.86-1.12). The risk of major bleeding may increase regardless of the severity of the disease (RR 1.78, 95% CI 1.15-2.74). The certainty of evidence is still low. Moderately affected COVID-19 patients may benefit from therapeutic anticoagulation, but the risk of bleeding is increased.

The emergence of coronavirus disease 2019 (COVID-19) has resulted in more than 300 million cases and 5 million deaths worldwide and innumerable economic losses. COVID-19 is acknowledged to transmit via air, but whether it is capable of transmitting via contaminated surfaces, also known as fomites, remains controversial. The overarching goal of this study was to investigate the presence and stability of SARS-CoV-2, the virus that causes COVID-19, on indoor surfaces and masks, and to provide insight into the possibility of fomite transmission. Since most transmission occurs indoors where humans spent 90% of their time, we first focused on quantifying the contamination level of SARS-CoV-2, including both viral RNA and viable virus, on commonly touched surfaces and in the heating, ventilation, and air cleaning (HVAC) systems in two university dormitories. Although we found up to 104 gene copies per ~10×10 cm2 on surfaces, we did not detect any viable virus, suggesting that the possibility of transmission via indoor surfaces is low. As universal masking has been recommended as an effective practice to prevent transmission of SARS-CoV-2, we shifted our focus to masks, both their effectiveness at filtering the virus from the air and their potential to serve as fomites. We evaluated the effectiveness of 11 face coverings for material filtration efficiency, inward protection efficiency on a manikin, and outward protection efficiency on a manikin. Masks made of filter materials, such as vacuum cleaner bag and HVAC filters, achieved a high material filtration efficiency whereas common textiles like cotton and acrylic usually showed the worst performance. The material filtration efficiency was generally positively correlated with either inward or outward protection effectiveness, but stiffer materials were an exception to this relationship as they did not fit as closely to the manikin's face and thus leaked substantially. Subsequently, we analyzed the survival of aerosolized SARS-CoV-2 in saliva on masks. Results suggested that the virus lost infectivity within one hour on an N95 respirator, surgical mask, polyester mask, and two types of cotton masks but not on a nylon/spandex mask. This study also highlighted the importance of applying virus in aerosols of realistic sizes when analyzing the stability of SARS-CoV-2 on surfaces. / Doctor of Philosophy / The emergence of coronavirus disease 2019 (COVID-19) has resulted in more than 300 million cases and 5 million deaths worldwide and innumerable economic losses. Researchers are debating if COVID-19 can transmit via surfaces contaminated with SARS-CoV-2, the virus that causes the disease. The goal of this study was to investigate whether SARS-CoV-2 is present and remains viable on indoor surfaces and masks, and to provide insight into the possibility of transmission via contaminated surfaces. Since most transmission occurs indoors where humans spent 90% of their time, we first focused on quantifying number of SARS-CoV-2 on commonly touched surfaces and in the heating, ventilation, and air cleaning (HVAC) systems in two university dormitories. Although we found a high concentration of SARS-CoV-2 genes on surfaces, we did not detect any viable virus, suggesting that the possibility of transmission via indoor surfaces is low. As universal masking has been recommended as an effective practice to prevent transmission of SARS-CoV-2, we shifted our focus to masks. We evaluated the effectiveness of 11 face coverings regarding their ability to trap viruses, protect wearers from inhaling viruses, and prevent infected individuals from expelling viruses into the surrounding air. Masks made of filter materials, such as a vacuum cleaner bag and HVAC filter, trapped the most viruses whereas common textiles like cotton and acrylic usually performed worst. It is also crucial that masks fit closely to the wearer's face to achieve better protection. Subsequently, we analyzed the ability of SARS-CoV-2 in aerosols, microscopic particles such as those exhaled by an infected person, to survive on different types of masks. Results suggested that the virus died within one hour on a majority of the masks. This study also highlighted the importance of applying aerosols of realistic sizes instead of large droplets when analyzing the survival of SARS-CoV-2 on surfaces.

Viral infection stimulates the immune response to produce many cytokines and chemokines, the proteins imperative to fight a brewing infection. This response begins through recognition of pathogen-associated molecular patterns (PAMPs) from the virus, or from other signatures characteristic of tissue damage, damage-associated molecular patterns (DAMPs), by pattern recognition receptors (PRRs) that in turn stimulate pro-inflammatory signaling cascades. The results of these signaling pathways include the release of cytokines and chemokines that work to further upregulate immune responses and attract immune cells to the site of infection, respectively. In the case of SARS-CoV-2 infection, these responses can become problematic if they go unmitigated or unresolved, resulting in the severe COVID-19 manifestation of the 'cytokine storm,' or multisystem inflammatory syndrome in children (MIS-C). One classically increased protein in cytokine storm of COVID-19 patients is C-X-C motif chemokine 10 (CXCL10), which has been explored as a prognostic marker as it is shown to be predictive of disease outcome in hospitalized patients. To prevent severe outcomes like cytokine storm, a delicate balance must be struck, to ensure that this inflammation does not result in high levels of diffuse tissue damage. To achieve this, anti-inflammatory pathways exist within the immune system and help dampen the signals being induced. One such unique anti-inflammatory protein is a pattern recognition receptor known as NLRX1 (Nucleotide binding oligomerization domain, leucine rich repeat containing X1), that can interact with two main pathways involved with anti-viral immunity, the NFB and interferon pathways, downregulating them to keep off-target tissue damage at bay. NLRX1 is also involved in several other cellular processes, including modulating cell death processes and cellular metabolism which can also impact viral replication and clearance indirectly. In this work, we investigated both the pro- and anti-inflammatory arms of the anti-SARS-CoV-2 response focusing on two key proteins – pro-inflammatory chemokine CXCL10 and immunoregulatory PRR NLRX1. The roles of these two proteins were explored utilizing transcriptomic analysis of both human and mouse RNA samples, immortalized cell culture work, humanized mouse models of SARS-CoV-2 infection, and mouse-adapted virus models to be able to utilize deficient mouse models. In this work we better characterize the immune response to SARS-CoV-2 and its related immune-driven pathobiology of disease. The data presented in this work continues to elucidate CXCL10's role as an important driver of viral clearance of SARS-CoV-2, translating data from human patient nasal swabs to the animal model of disease, exploring differential inflammation and immune responses in the absence of CXCL10. Additionally, the work shown here provides further understanding of NLRX1 and its role in antiviral immunity with the context of SARS-CoV-2 infection. The interactions between this protein and the virus remains to be fully characterized, however, it appears they have some degree of mutual inhibition as determined by animal and cell culture models. The culmination of work here emphasizes the importance for both the pro- and anti-inflammatory responses in SARS-CoV-2 infection and offers insight into two possible related targets for future drug development. / Doctor of Philosophy / When a virus invades the body, the immune system kicks off many signaling cascades to keep the virus from replicating, clear virus already established in cells, and clean up the tissues surrounding the infected area of the remnants of cells that already succumbed to the virus. While this immune response is important to fight off the virus that has made its way into the body, overactive immune responses can result in hospital stays requiring supportive care to aid recovery from possible off-target tissue damage. One such case of this happening is when SARS-CoV-2 induces such a strong response, the immune system becomes overzealous and results in overproduction of pro-inflammatory cytokines and chemokines, signaling proteins in the immune system, which can lead to the characteristic 'cytokine storm' of severe COVID-19 disease. One of the proteins most often overproduced is the chemokine CXCL10, and this protein has been used as a biomarker in clinical practice to successfully predict severe disease outcomes in COVID-19 patients. To help combat severe disease outcomes and high levels of tissue damage, the immune system has inborn checks and balances to ensure that proteins like CXCL10 do not reach the level of overproduction as in the cytokine storm of COVID-19. One of these natural checkpoints is a protein called NLRX1, which interacts with two of the main pathways that can lead to the overproduction of cytokines seen overproduced in the case of cytokine storm. NLRX1 also has other roles in other interesting facets important for viral infections, including the metabolism of the cell and cellular death processes. The culmination of these roles could offer up NLRX1 as a possible target for treatments in the future. The work put together here explores both sides of the immune response, turning it 'on' with pro-inflammatory signaling, and turning it 'off' with anti-inflammatory signaling, trying to find just the right amount of inflammation to clear a viral invader while also impeding off target and diffuse tissue damage as the body fights the virus. This work focuses on two key proteins, CXCL10 to represent pro-inflammatory responses, and NLRX1 to represent the anti-inflammatory signaling. Understanding both arms of the immune response to SARS-CoV-2 infection is crucial to being able to identify potential targets for future treatments to help combat severe outcomes of SARS-CoV-2 infection. Using multiple levels across the translational spectrum, including cell culture, animal models, and human patient RNA from COVID test swabs, we explore both facets of SARS-CoV-2 immunity, focusing on these two proteins. Utilizing mouse models bearing deletions of the genes required to make these proteins and a mouse-adapted strain of SARS-CoV-2, this work characterizes how important these individual proteins are in the immune response to SARS-CoV-2, and work as proxies to understand the broader impacts of either the positive or negative regulation of immune signaling. Because of the work culminated here, these two tangentially related proteins are also offered up as possible future drug targets for the development of treatments in severe COVID-19 disease with cytokine storm presentation.

The late 2019 marked the onset of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that led to the unprecedented COVID-19 pandemic, with profound global health and socioeconomic impacts. This thesis offers a thorough examination of the molecular biology, evolution, and disease-causing mechanisms of SARS-CoV-2, as well as recent advancements in understanding the structural and functional implications of mutations in viral proteins. The prevailing belief is that SARS-CoV-2 originated from a zoonotic transmission involving bats as the natural reservoir hosts, with an unknown intermediate host facilitating transmission to humans. Genomic sequencing and phylogenetic analysis have identified similarities between SARS-CoV-2 and bat coronaviruses, particularly RaTG13, indicating a potential bat origin. However, the exact circumstances and intermediate hosts of the spillover event remain under investigation. In its structure, SARS-CoV-2 is an enveloped virus with a positive-sense single-stranded RNA genome. This genome encodes both structural and non-structural proteins crucial for viral replication and the development of the disease. The spike (S) protein facilitates viral entry by binding to the angiotensin-converting enzyme 2 (ACE2) receptor. Meanwhile, non-structural proteins are involved in viral RNA synthesis, immune evasion, and the assembly of virions. Alterations in the genetic makeup of the SARS-CoV-2 genome, notably within the spike protein, can impact transmission efficiency, viral load, and immune evasion. Notable mutations such as D614G, N501Y, and E484K have been associated with increased transmissibility and reduced neutralization by antibodies. Understanding the effects of these mutations on viral fitness and pathogenicity is crucial for informing public health interventions and vaccine development efforts. The impacts of Non-structural proteins (NSPs) on viral replication and transmission are however understudied. In this study, we focused on mutations in the several NSPs including NSP1, 2, 3, 13,14, and 15 of the early Omicron (BA.1) and XBB 1.5 variants and investigated their impact on structure and the functional implications using bioinformatics tools and protein structure prediction methods. Our analysis focused on potential alterations in NSP1's structure and hence its ability to suppress host gene expression and modulate immune responses, shedding light on the mechanisms by which SARS-CoV-2 evolves to evade host defenses. Overall, this thesis gives insights into the emergence, structure, replication cycle, evolution, and pathogenesis of SARS-CoV-2, highlighting the importance of ongoing research efforts in understanding and combatting this global health threat and provides a detailed structural analysis of mutations in NSPs. / Master of Science / The COVID-19 pandemic, instigated by the virus referred to as SARS-CoV-2, is a novel coronavirus believed to have originated in bats and possibly transmitted to humans via an intermediate host. Its genetic structure and protein interactions play crucial roles in how it spreads and causes illness. We need to understand where the virus came from, how it's built, it's life cycle and how it's changing over time. While the virus has undergone a lot of mutations over time, scientists are actively studying these changes, with a lot of focus on the structural ones, to understand their implications for public health measures and vaccine development. In our study, we focus on the non- structural proteins and aim to investigate the effect of selected mutations on the protein structure and function using bioinformatics. Understanding the virus is essential for effectively combating future pandemics and safeguarding public health.

Yes / Since December 2019, a new type of coronavirus called novel coronavirus (2019-nCoV, or COVID-19) was identified in Wuhan, China and on March 11, 2020, the World Health Organization (WHO) has declared the novel coronavirus (COVID-19) outbreak a global pandemic. With more than 101,797,158 confirmed cases, resulting in 3,451,354 deaths as of May 21, 2021, the world faces an unprecedented economic, social, and health impact. The clinical spectrum of COVID-19 has a wide range of manifestations, ranging from an asymptomatic state or mild respiratory symptoms to severe viral pneumonia and acute respiratory distress syndrome. Several diagnostic methods are currently available for detecting the coronavirus in clinical, research, and public health laboratories. Some tests detect the infection directly by detecting the viral RNA using real time reverse transcriptase polymerase chain reaction (RT-PCR) and other tests detect the infection indirectly by detecting the host antibodies. Additional techniques are using medical imaging diagnostic tools such as X-ray and computed tomography (CT). Various approaches have been employed in the development of COVID-19 therapies. Some of these approaches use drug repurposing (eg Remdesivir and Dexamethasone) and combinational therapy (eg Lopinavir/Ritonavir), whilst others aim to develop anti-viral vaccines (eg mRNA and antibody). Additionally, health experts integrate data sharing, provide with guidelines and advice to minimize the effects of the pandemic. These guidelines include wearing masks, avoiding direct contact with infectious people, respiratory and personal hygiene.

The human gastrointestinal (GI) tract is a highly heterogeneous system composed of several distinct regions that differ in structure, function and cellular diversity. The presence of distinct cellular populations greatly affects host factor expres- sion and limits pathogen tropism in the GI tract. However, there is a lack of understanding of how GI epithelium heterogeneity affects Helicobacter pylori (H. pylori ) and SARS-CoV-2 infections in the GI tract. This thesis focused on examining the effect of gastric epithelium heterogeneity on H. pylor i infection and the impact of differential expression of ACE2 on SARS- CoV-2 infection in the GI tract. Although it was known that H. pylori colocalizes with pit cells in the gastric gland, a cell type-specific tropism of H. pylori has not been identified. Using gastric organoid-derived monolayers and single-cell RNA sequencing, this work identifies MUC5AC positive pit cell subpopulation as preferential attachment sites for H. pylori in gastric epithelium. The preference of H. pylori for highly differentiated pit cells was verified in tissue biopsies of H. pylori -infected patients. The second project included in this thesis focused on the differential susceptibil- ity of GI organoid-derived monolayers to SARS-CoV-2, the causative agent of the COVID-19 pandemic. Similarly to previously published data, SARS-CoV-2 ex- hibited a strong tropism to small intestine organoid-derived monolayers, whereas corpus organoid-derived monolayers were not infected by SARS-CoV-2. In addi- tion, a correlation between the differential susceptibility of GI organoid-derived monolayers to SARS-COV-2 infection and GI tract segment-specific ACE2 ex- pression patterns was observed. The ectopic expression of ACE2 in adult corpus organoid-derived monolayers resulted in susceptibility of adult gastric cells to SARS-CoV-2 infection. In summary, the GI epithelium and thus host factor expression are highly hetero- geneous at the cellular level, which greatly influences the infection with H. pylori and SARS-CoV-2 in the GI tract. The data presented in this thesis contributes to a better understanding of GI epithelium heterogeneity and provides a stepstone for further research into host-pathogen interactions in the GI tract. / Der menschliche Gastrointestinaltrakt (GI-Trakt) ist ein hoch heterogenes Sys- tem und zusammengesetzt aus mehreren distinkten Regionen, die sich in Struktur, Funktion und zellul¨arer Diversit¨at unterscheiden. Das Auftreten unterschiedlicher Zellpopulationen beeinflusst die Expression von Wirtsfaktoren erheblich und lim- itiert den Tropismus von Krankheitserregern im GI-Trakt. Wie die Heterogenit¨at des GI Epitheliums Helicobacter pylori (H. pylori) und SARS-CoV-2 Infektionen im GI-Trakt beeinflusst, ist jedoch nur mangelhaft verstanden. Diese Thesis fokussiert sich auf die Examinierung des Effekts der Heterogenit¨at von gastrischem Epithelium im Kontext von H. pylori Infektionen, sowie den Ein- fluss der Expression von ACE2 bei SARS-CoV-2 Infektionen im GI-Trakt. Bekan- ntermaßen kolokalisiert H. pylori mit Zellen, genannt ”pit cells“, in der Magen- dr¨use, bislang wurde ein Zelltyp-spezifischer Tropismus jedoch nicht identifiziert. Durch die Verwendung von gastrischen Organoid-abgeleiteten Monoschichten (gastric organoid-derived monolayers) und Einzelzell-RNA-Sequenzierung (single- cell RNA-sequencing) identifiziert diese Arbeit MUC5AC positive pit cell Sub- populationen als pr¨aferierte Anheftungsstelle von H. pylori in gastrischem Ep- ithelium. Die Pr¨aferenz von H. pylori f¨ur hoch differenzierte pit cells wurde in Gewebsbiopsien von H. pylori infizierten Patienten verifiziert. Das zweite Projekt dieser Thesis fokussiert sich auf die differenzielle Suszepti- bilit¨at von gastrointestinalen organoid-derived monolyers f¨ur SARS-CoV-2, der kausative Krankheitserreger der COVID-19 Pandemie. ¨Ahnlich zu publizierten Daten weist SARS-CoV-2 einen starken Tropismus f¨ur Monoschichten aus D¨un- ndarmorganoiden auf, wohingegen Monoschichten aus Korpusorganoiden nicht in- fiziert wurden. Dar¨uber hinaus wurde eine Korrelation zwischen der differenziellen Suszeptibilit¨at von gastrointestinalen organoid-derived monolayers f¨ur eine SARS- CoV-2 Infektion und GI-Trakt Segment-spezifischen ACE2 Expressionsmustern beobachtet. Die ektopische Expression von ACE2 in Monoschichten aus adulten Korpusorganoiden resultierte in Suszeptibilit¨at adulter gastrischen Zellen f¨ur eine SARS-CoV-2 Infektion. Zusammenfassend ist das GI-Epithelium und somit die Expression von Wirtsfaktoren auf zellul¨arer Ebene hoch heterogen, was die Infektion des GI-Trakts mit H. pylori und SARS-CoV-2 stark beeinflusst. Die generierten Daten diese Arbeit tragen zu einem besseren Verst¨andnis der Heterogenit¨at des GI-Epitheliums bei und bilden eine Basis f¨ur weitere Forschung der Wirts-Pathogen-Interaktion im GI-Trakt.

Das severe acute respiratory syndrome Coronavirus (SARS-CoV) ist ein hochpathogenes Virus, dessen zoonotischer Eintrag in die Bevölkerung eine substantielle Gesundheitsgefahr darstellt. Die Identifizierung von Wirtszellfaktoren, die für die SARS-CoV-Ausbreitung und Pathogenese wichtig sind, könnte neue Ansatzpunkte für die Therapie liefern. Das SARS-CoV-Oberflächenprotein Spike (S) bindet an den zellulären Rezeptor angiotensin converting Enzyme 2 (ACE2) und vermittelt den viralen Eintritt in Zielzellen. Die Spaltung und Aktivierung des S Proteins durch Wirtszellproteasen ist für den infektiösen, S Protein-vermittelten Zelleintritt von SARS-CoV essentiell. Die Typ II Transmembranserinproteasen (TTSPs) TMPRSS2 und HAT spalten und aktivieren das S Protein, zumindest nach gerichteter Expression in Zelllinien. Ob diese Enzyme in der menschlichen Lunge, den Zielzellen der SARS-CoV-Infektion, exprimiert werden, war jedoch unklar und sollte im Rahmen der vorliegenden Arbeit untersucht werden. TMPRSS2 und HAT spalten auch den viralen Rezeptor ACE2 und es wurde postuliert, dass die ACE2-Spaltung den viralen Eintritt erhöht. Der zugrundeliegende Mechanismus war jedoch nicht bekannt und sollte innerhalb der vorliegenden Arbeit aufgeklärt werden. Es konnte gezeigt werden, dass TMPRSS2 und HAT zusammen mit ACE2 in Epithelzellen des Respirationstrakts exprimiert werden. Die Proteasen könnten daher die Ausbreitung von SARS-CoV im Lungenepithel fördern. Weiterhin wurde eine Aminosäuresequenz in ACE2 identifiziert, die für die Prozessierung durch TMPRSS2 und HAT essentiell ist. Die funktionelle Analyse von ACE2- Mutanten zeigte, dass die Spaltung in diesem Bereich infektionsverstärkend wirkt. Immunfluoreszenz-Studien erbrachten Hinweise darauf, dass die Verstärkung der Infektion auf eine erhöhte Aufnahme von Virus-Partikeln in die Zelle zurückzuführen ist. Schließlich konnte demonstriert werden, dass TMPRSS2 und eine weitere zelluläre Protease, A Disintegrin And Metalloproteinase 17 (ADAM17), um die ACE2-Spaltung konkurrieren und die ADAM17- Spaltstelle in ACE2 konnte kartiert werden. Die ACE2-Spaltung durch ADAM17 war jedoch für den S Protein-getriebenen Zelleintritt verzichtbar. Zusammenfassend zeigen diese Untersuchungen, dass TMPRSS2 und HAT die SARS-CoV-Infektion durch Spaltung von S Protein und Rezeptor fördern. Die Proteasen stellen daher mögliche Angriffspunkte für die antivirale Intervention dar.

Introducción. El COVID-19 y la gestación es una nueva intercurrencia en la valoración de riesgos para la atención de la gestante. Desde el inicio de la pandemia en el país, los casos han ido en aumento. El primer caso atendido en el Hospital San Bartolomé fue el 12 de abril. Desde los primeros reportes de gestantes COVID+ en China, a la fecha, se tiene cada vez mayor información, siendo importante para fines del manejo de la gestante COVID+ que se conozca su epidemiología y los resultados perinatales. Objetivo. Determinar la epidemiología y resultados materno perinatales de COVID-19 en las gestantes del Hospital Nacional Docente Madre Niño San Bartolomé, Lima, Perú. Método. Estudio observacional de corte transversal, en los meses de abril a julio 2020. Se incluyó a todas las gestantes que llegaron a la emergencia obstétrica del Hospital San Bartolomé, a las cuales se les realizó una prueba de inmunocromatografía para IgM/IgG, para determinar la seroprevalencia de COVID-19. Las variables obstétricas y perinatales fueron recolectadas en una ficha de datos al ingreso a la emergencia. Resultados. Se realizó prueba rápida para SARS-CoV-19 a 345 gestantes que se hospitalizaron para atención de parto. La edad promedio fue 27 años, con 10% de adolescentes y 16% de mayores de 35 años; 60% tenía 2 a 4 embarazos, 38% de los partos fue vaginal, 15% de ellos pretérmino; 1,2% de las gestantes fue sintomática y 0,2% ingresó a la unidad de cuidados intensivos. El 61% de los recién nacidos pesó entre 2 500 y 3 500 g, 53% fue sexo masculino, 94% tuvo Apgar mayor de 7 al minuto, 3,3% con hisopado positivo dentro de las primeras 24 horas. Se presentaron 3% de óbitos. El 48% de las gestantes provino del Cono Norte de la ciudad de Lima. Conclusiones. Casi 100% de las gestantes fue asintomática y solo 0,2% tuvo complicaciones respiratorias. La culminación del parto por vía cesárea fue baja en relación a otras publicaciones; el motivo de cesárea fue por indicación obstétrica. Escaso número de neonatos tuvo hisopado positivo. Hubo mayor incidencia de óbitos en julio 2020. El mayor porcentaje de pacientes provino del Cono Norte de Lima. / Introduction: COVID-19 and pregnancy is a new intercurrence in risk assessment for the care of the pregnant woman. Since the beginning of the pandemic in the country, cases have been increasing. The first case attended at the San Bartolomé Hospital was on April 12. Since the first reports of COVID+ pregnant women in China, to date, there is more important information on epidemiology and perinatal results for the management of the COVID+ pregnant woman. Objective: To determine the epidemiology and maternal perinatal outcomes of COVID-19 in pregnant women at the Hospital Nacional Docente Madre Niño San Bartolomé, Lima, Peru. Methods: Observational cross-sectional study, from April to July 2020. All the pregnant women who arrived at the obstetric emergency at Hospital San Bartolomé were included, and they underwent an immunochromatography test for IgM / IgG, to determine the seroprevalence of COVID-19. Obstetric and perinatal variables were collected in a data sheet upon admission to the emergency room. Results: Rapid test for SARS-CoV-19 was performed in 345 pregnant women who were hospitalized for delivery care. The average age was 27 years, with 10% adolescents and 16% over 35 years; 60% had 2 to 4 pregnancies, 38% of deliveries were vaginal, 15% of them preterm; 1.2% of the pregnant women were symptomatic and 0.2% were admitted to the intensive care unit. 61% of the newborns weighed between 2 500 and 3 500 g, 53% were male, 94% had an Apgar score greater than 7 at one minute, 3.3% with a positive swab within the first 24 hours. There were 3% fetal deaths. 48% of the pregnant women came from the Northern Cone of the city of Lima. Conclusions: Almost 100% of the pregnant women were asymptomatic and only 0.2% had respiratory complications. The mode of delivery by cesarean section was low in relation to other publications, all had obstetric indication. A small number of neonates had a positive swab. There was a higher incidence of fetal deaths in July 2020. The highest percentage of patients came from the Northern Cone of Lima.

The aim of this diploma thesis was to describe information about SARS-CoV-2 virus and coronavirus disease (COVID-19), to evaluate the course of the disease in the Home with a special regime in Břevnice, in which the epidemic took place at the beginning of the first wave of COVID-19 pandemic in spring 2020. Another goal was to perform an antibody analysis and evaluate the obtained data. I divided the diploma thesis into three main parts: theoretical, experimental and discussion. In the theoretical part, I worked with the literature and described information related not only to COVID-19, but also to other serious infections caused by human coronaviruses. In the experimental part, which I performed in the immunological laboratory of the Department of Joint Laboratories at Havlíčkův Brod Hospital, I dealt with the issue of the clinical course of the disease, the severity of the disease and possible consequences after the infection. I also dealt with methods for the determination of antibodies, the principles of which are described in Chapter 4.5. The diagnostic methods and procedures used are described in Chapter 5.3 Laboratory Assays. From the obtained data, I prepared graphs and tables and processed data on the clinical course of the infection in the Břevnice Home, both for the clients and the...

Se validó y evaluó un método de RT-PCR en tiempo real usando cebadores y sondas específicas para los genes RdRP de SARS-CoV-2 y GAPDH de humanos; este último fue usado como control endógeno. Se evaluó la especificidad y sensibilidad; además, se evaluó otros parámetros como la robustez, la repetibilidad, reproducibilidad, comparabilidad y el límite de detección. La sensibilidad, especificidad, los valores predictivos positivo y negativo, la robustez, comparabilidad y la repetibilidad-reproducibilidad de la prueba de RT-PCR en tiempo real dúplex fue de 100%, con un límite de detección de 100 copias/μL, de acuerdo con los criterios de aceptación establecidos para validación del protocolo. Esta prueba estandarizada es una buena alternativa para el diagnóstico de COVID-19; además, la prueba fue aplicada de manera exitosa en personas sospechosas de la enfermedad permitiendo controlar el número de falsos negativos.