Продолжительное выделение коронавируса
May. 18th, 2022 11:07 pm![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png)
Статья, в которой речь идет о том, что у тех, кто переболел ковидом, легко и умеренно, коронавирус САРС2 выделяется со стулом до 7 месяцев. Проверили до 300 дней. Первые выделения вируса со стулом отметили через 3 дня после положительного теста.
Спустя 4 месяца, ни один из переболевших не выделял вирус в носоглотке (но дольше 4 мес не проверяли). А в фекальном материале вирус содержался у 13%. Спустя 7 месяцев- у 4%.
Данные собраны по 113 людям.
Авторы склоняются к мысли, что коронавирусная инфекция иногда долго персистирует в жкт. Об этом в "дискуссии".
Зачастую те, у кого выделяется вирус, в опросниках отмечали, что имели разные проблемы с жкт (но не диаррею). Однако часть была асимптоматичная. Тем не менее, авторы думают, что за симптоматичность жкт отвечал вирус, хоть это всего лишь корреляция.
Лабораторные исследования о том, что вирус может поражать ткани жкт, есть, но для подтверждения явления у людей, надо было бы брать биопсию, что пока не делается.
То, что это было не "очищение" остаточных копий вируса в организме- понятно по тому, что продолжалось выделение долго, и количества вирусной РНК были довольно большие. К тому же, ученые из Стенфорда дополнительно меряли субгеномную РНК, показатель активно делящегося вируса.
Авторы не знают, на сколько выделяющиеся вирусы могут заражать (вдруг что), тк образцы кала специально обеззараживались, и не могут с уверенностью показать что это не регулярные реинфекции (тк за время исследования образцы собирали не каждый день, а с перерывами, иногда в несколько месяцев), но склоняются к мысли про персистенцию. Есть шанс, что персистенция вируса может быть причиной и долгого ковида.
COVID-19 is a disease with protean manifestations, ranging from respiratory to gastrointestinal to systemic. Although the primary site of SARS-CoV-2 infection is the respiratory tract, the presence of symptoms affecting other organ systems (e.g., abdominal pain, nausea, arthralgia), coupled with in vitro evidence of SARS-CoV-2 infectivity in a variety of other tissues, suggests that SARS-CoV-2 infection can extend beyond the respiratory system. Meta-analyses of studies that focus on hospitalized individuals with COVID-19 estimate the pooled incidence of gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea to be between 11% and 18%.1,2,3,6, 7, 8 Additionally, within this moderate- to severe-disease group, SARS-CoV-2 RNA has been detected in 40%–85% of fecal samples (reviewed in Brooks EF and Bhatt AS9), indicating that SARS-CoV-2 viral RNA is found in feces nearly as frequently as in respiratory secretions.10 Patients with moderate to severe COVID-19 have been well studied; by contrast, much less is known about the clearance of SARS-CoV-2 RNA in the feces of patients with mild to moderate disease despite the fact that they make up ∼81% of those who contract COVID-19.11,12 Furthermore, most studies are cross-sectional, and the few reported longitudinal studies have focused on the early time period after diagnosis. Thus, a comprehensive understanding of the dynamics of fecal clearance of SARS-CoV-2 RNA in individuals with mild to moderate COVID-19 is both of crucial importance and lacking.
Interestingly, in the few studies that have investigated longitudinal fecal samples, prolonged fecal shedding of SARS-CoV-2 RNA can occur even after respiratory shedding ceases. Indeed, in one notable pediatric case, fecal viral RNA shedding extended beyond 70 days after disease onset.8 If SARS-CoV-2 RNA shedding in the feces is indicative of a GI infection, this suggests that SARS-CoV-2 infection of the GI tract can continue after clearance from the respiratory tract.
While the presence of SARS-CoV-2 RNA in feces is well established, whether live, infectious SARS-CoV2 is commonly shed in stool remains an outstanding question (reviewed in Guo M et al.13). Five studies have reported isolating infectious SARS-CoV-2 from stool samples collected from participants with severe COVID-19,14, 15, 16, 17, 18 whereas others have reported being unable to isolate infectious virions from stool.19,20 Therefore, it remains unclear whether the presence of infectious virions of SARS-CoV-2 in the stool is a rare or common phenomenon. However, there is mounting evidence of possible SARS-CoV-2 infection of the GI tract. Specifically, the presence of SARS-CoV-2 RNA,4,21, 22, 23protein antigen,21,24 and virions4,23,25 in GI biopsies all point to a potential infection of the GI tract. Additionally, the presence of a gut immune response26 and inflammation markers such as fecal calprotectin27,28 in individuals with COVID-19 provides supporting evidence of a GI infection. Finally, in vitro experiments reveal that SARS-CoV-2 is able to successfully infect enteroid models of the gut29, 30, 31 and intestinal cell lines.32 This phenomenon of possible GI tract involvement is not surprising, as bovine coronavirus (BCoV) and human enteric coronavirus (HECoV-4408), both of the same genus as SARS-CoV-2 (Betacoronaviruses), can infect respiratory and GI tissues.33 Taken together, these data indicate that the GI tract may be an important site of SARS-CoV-2 infection.33 SARS-CoV-2 presence in the GI tract has additional relevance to patient health. The GI tract is a highly immunoactive tissue, and SARS-CoV-2 antigens in this body site may hone a humoral immune response against variants of the SARS-CoV-2 virus.21 Furthermore, prolonged presence of SARS-CoV-2 in the GI tissue may also have an impact on the hitherto mysterious phenomenon of post-acute sequelae of SARS-CoV-2 infection (PASC) or “Long COVID,” where individuals suffer from an unusual constellation of symptoms even after recovery from the respiratory SARS-CoV-2 infection.34 Taken together, it is critical that we understand whether or not the GI tract is infected and the dynamics of the infection in this tissue, from the standpoint of both the acute infection and the long-term sequelae of COVID-19.
Here, we sought to better define the features of SARS-CoV-2 presence in the GI tract and its relevance for short- and long-term human health. We leveraged longitudinal fecal and respiratory samples from individuals enrolled in a randomized controlled study of Peg-interferon lambda-1a (IFN-λ) versus a placebo control for the treatment of mild to moderate COVID-19 (n = 120).35 While the intervention did not shorten the duration of oropharyngeal shedding of SARS-CoV-2 RNA (primary outcome) or disease symptoms (secondary outcome), the study provided a rich, prospectively collected dataset from which to evaluate fecal shedding dynamics and its relation to GI symptoms.
Using fecal samples collected at regular intervals from the time of COVID-19 diagnosis to 10 months after diagnosis, we compared fecal viral RNA shedding with the presence of GI and other symptoms and found that it is positively correlated with GI symptoms. This constitutes the largest longitudinal analysis of paired fecal viral RNA shedding and disease symptomatology data in individuals with mild to moderate COVID-19, and it reveals important information about the pathophysiology of the disease.
Gastrointestinal symptoms and SARS-CoV-2 RNA shedding in feces point to the gastrointestinal tract as a possible site of infection in COVID-19. Researchers from Stanford University measured the dynamics of fecal viral RNA in patients with mild to moderate COVID-19 followed for 10 months post-diagnosis. The authors found that fecal viral RNA shedding was correlated with gastrointestinal symptoms in patients who had cleared their respiratory infection. They also observed that fecal shedding can continue to 7 months post-diagnosis. In conjunction with recent related findings, this work presents compelling evidence of SARS-CoV-2 infection in the gastrointestinal tract and suggests a possible role for long-term infection of the gastrointestinal tract in syndromes such as “long COVID.”
COVID-19 manifests with respiratory, systemic, and gastrointestinal (GI) symptoms.1, SARS-CoV-2 RNA is detected in respiratory and fecal samples, and recent reports demonstrate viral replication in both the lung and intestinal tissue.2, 3, 4 Although much is known about early fecal RNA shedding, little is known about long-term shedding, especially in those with mild COVID-19. Furthermore, most reports of fecal RNA shedding do not correlate these findings with GI symptoms.5.
Fecal SARS-CoV-2 RNA is detected in 49.2% [95% confidence interval, 38.2%–60.3%] of participants within the first week after diagnosis. Whereas there was no ongoing oropharyngeal SARS-CoV-2 RNA shedding in subjects at 4 months, 12.7% [8.5%–18.4%] of participants continued to shed SARS-CoV-2 RNA in the feces at 4 months after diagnosis and 3.8% [2.0%–7.3%] shed at 7 months. Finally, we found that GI symptoms (abdominal pain, nausea, vomiting) are associated with fecal shedding of SARS-CoV-2 RNA.
Спустя 4 месяца, ни один из переболевших не выделял вирус в носоглотке (но дольше 4 мес не проверяли). А в фекальном материале вирус содержался у 13%. Спустя 7 месяцев- у 4%.
Данные собраны по 113 людям.
Авторы склоняются к мысли, что коронавирусная инфекция иногда долго персистирует в жкт. Об этом в "дискуссии".
Зачастую те, у кого выделяется вирус, в опросниках отмечали, что имели разные проблемы с жкт (но не диаррею). Однако часть была асимптоматичная. Тем не менее, авторы думают, что за симптоматичность жкт отвечал вирус, хоть это всего лишь корреляция.
Лабораторные исследования о том, что вирус может поражать ткани жкт, есть, но для подтверждения явления у людей, надо было бы брать биопсию, что пока не делается.
То, что это было не "очищение" остаточных копий вируса в организме- понятно по тому, что продолжалось выделение долго, и количества вирусной РНК были довольно большие. К тому же, ученые из Стенфорда дополнительно меряли субгеномную РНК, показатель активно делящегося вируса.
Авторы не знают, на сколько выделяющиеся вирусы могут заражать (вдруг что), тк образцы кала специально обеззараживались, и не могут с уверенностью показать что это не регулярные реинфекции (тк за время исследования образцы собирали не каждый день, а с перерывами, иногда в несколько месяцев), но склоняются к мысли про персистенцию. Есть шанс, что персистенция вируса может быть причиной и долгого ковида.
COVID-19 is a disease with protean manifestations, ranging from respiratory to gastrointestinal to systemic. Although the primary site of SARS-CoV-2 infection is the respiratory tract, the presence of symptoms affecting other organ systems (e.g., abdominal pain, nausea, arthralgia), coupled with in vitro evidence of SARS-CoV-2 infectivity in a variety of other tissues, suggests that SARS-CoV-2 infection can extend beyond the respiratory system. Meta-analyses of studies that focus on hospitalized individuals with COVID-19 estimate the pooled incidence of gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea to be between 11% and 18%.1,2,3,6, 7, 8 Additionally, within this moderate- to severe-disease group, SARS-CoV-2 RNA has been detected in 40%–85% of fecal samples (reviewed in Brooks EF and Bhatt AS9), indicating that SARS-CoV-2 viral RNA is found in feces nearly as frequently as in respiratory secretions.10 Patients with moderate to severe COVID-19 have been well studied; by contrast, much less is known about the clearance of SARS-CoV-2 RNA in the feces of patients with mild to moderate disease despite the fact that they make up ∼81% of those who contract COVID-19.11,12 Furthermore, most studies are cross-sectional, and the few reported longitudinal studies have focused on the early time period after diagnosis. Thus, a comprehensive understanding of the dynamics of fecal clearance of SARS-CoV-2 RNA in individuals with mild to moderate COVID-19 is both of crucial importance and lacking.
Interestingly, in the few studies that have investigated longitudinal fecal samples, prolonged fecal shedding of SARS-CoV-2 RNA can occur even after respiratory shedding ceases. Indeed, in one notable pediatric case, fecal viral RNA shedding extended beyond 70 days after disease onset.8 If SARS-CoV-2 RNA shedding in the feces is indicative of a GI infection, this suggests that SARS-CoV-2 infection of the GI tract can continue after clearance from the respiratory tract.
While the presence of SARS-CoV-2 RNA in feces is well established, whether live, infectious SARS-CoV2 is commonly shed in stool remains an outstanding question (reviewed in Guo M et al.13). Five studies have reported isolating infectious SARS-CoV-2 from stool samples collected from participants with severe COVID-19,14, 15, 16, 17, 18 whereas others have reported being unable to isolate infectious virions from stool.19,20 Therefore, it remains unclear whether the presence of infectious virions of SARS-CoV-2 in the stool is a rare or common phenomenon. However, there is mounting evidence of possible SARS-CoV-2 infection of the GI tract. Specifically, the presence of SARS-CoV-2 RNA,4,21, 22, 23protein antigen,21,24 and virions4,23,25 in GI biopsies all point to a potential infection of the GI tract. Additionally, the presence of a gut immune response26 and inflammation markers such as fecal calprotectin27,28 in individuals with COVID-19 provides supporting evidence of a GI infection. Finally, in vitro experiments reveal that SARS-CoV-2 is able to successfully infect enteroid models of the gut29, 30, 31 and intestinal cell lines.32 This phenomenon of possible GI tract involvement is not surprising, as bovine coronavirus (BCoV) and human enteric coronavirus (HECoV-4408), both of the same genus as SARS-CoV-2 (Betacoronaviruses), can infect respiratory and GI tissues.33 Taken together, these data indicate that the GI tract may be an important site of SARS-CoV-2 infection.33 SARS-CoV-2 presence in the GI tract has additional relevance to patient health. The GI tract is a highly immunoactive tissue, and SARS-CoV-2 antigens in this body site may hone a humoral immune response against variants of the SARS-CoV-2 virus.21 Furthermore, prolonged presence of SARS-CoV-2 in the GI tissue may also have an impact on the hitherto mysterious phenomenon of post-acute sequelae of SARS-CoV-2 infection (PASC) or “Long COVID,” where individuals suffer from an unusual constellation of symptoms even after recovery from the respiratory SARS-CoV-2 infection.34 Taken together, it is critical that we understand whether or not the GI tract is infected and the dynamics of the infection in this tissue, from the standpoint of both the acute infection and the long-term sequelae of COVID-19.
Here, we sought to better define the features of SARS-CoV-2 presence in the GI tract and its relevance for short- and long-term human health. We leveraged longitudinal fecal and respiratory samples from individuals enrolled in a randomized controlled study of Peg-interferon lambda-1a (IFN-λ) versus a placebo control for the treatment of mild to moderate COVID-19 (n = 120).35 While the intervention did not shorten the duration of oropharyngeal shedding of SARS-CoV-2 RNA (primary outcome) or disease symptoms (secondary outcome), the study provided a rich, prospectively collected dataset from which to evaluate fecal shedding dynamics and its relation to GI symptoms.
Using fecal samples collected at regular intervals from the time of COVID-19 diagnosis to 10 months after diagnosis, we compared fecal viral RNA shedding with the presence of GI and other symptoms and found that it is positively correlated with GI symptoms. This constitutes the largest longitudinal analysis of paired fecal viral RNA shedding and disease symptomatology data in individuals with mild to moderate COVID-19, and it reveals important information about the pathophysiology of the disease.
Gastrointestinal symptoms and SARS-CoV-2 RNA shedding in feces point to the gastrointestinal tract as a possible site of infection in COVID-19. Researchers from Stanford University measured the dynamics of fecal viral RNA in patients with mild to moderate COVID-19 followed for 10 months post-diagnosis. The authors found that fecal viral RNA shedding was correlated with gastrointestinal symptoms in patients who had cleared their respiratory infection. They also observed that fecal shedding can continue to 7 months post-diagnosis. In conjunction with recent related findings, this work presents compelling evidence of SARS-CoV-2 infection in the gastrointestinal tract and suggests a possible role for long-term infection of the gastrointestinal tract in syndromes such as “long COVID.”
COVID-19 manifests with respiratory, systemic, and gastrointestinal (GI) symptoms.1, SARS-CoV-2 RNA is detected in respiratory and fecal samples, and recent reports demonstrate viral replication in both the lung and intestinal tissue.2, 3, 4 Although much is known about early fecal RNA shedding, little is known about long-term shedding, especially in those with mild COVID-19. Furthermore, most reports of fecal RNA shedding do not correlate these findings with GI symptoms.5.
Fecal SARS-CoV-2 RNA is detected in 49.2% [95% confidence interval, 38.2%–60.3%] of participants within the first week after diagnosis. Whereas there was no ongoing oropharyngeal SARS-CoV-2 RNA shedding in subjects at 4 months, 12.7% [8.5%–18.4%] of participants continued to shed SARS-CoV-2 RNA in the feces at 4 months after diagnosis and 3.8% [2.0%–7.3%] shed at 7 months. Finally, we found that GI symptoms (abdominal pain, nausea, vomiting) are associated with fecal shedding of SARS-CoV-2 RNA.
no subject
Date: 2022-05-19 06:49 am (UTC)no subject
Date: 2022-05-19 06:53 am (UTC)no subject
Date: 2022-05-19 03:40 pm (UTC)no subject
Date: 2022-05-19 10:53 pm (UTC)фекально-оральный путь- довольно распространенный (грязные руки, аэросолизация в общественном туалете) и неплохо работает для тех микробов, что устойчивы к выживанию в среде.
коронавирус, не герой в этом деле, но в пределах нескольких дней- может.
САРС 2 заразнее чем САРС на порядок а то и больше, и более усточив в среде.
то что это реально- посмотри как передавался САРС в свое время в ГонКонге-
Amoy gardenы
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC539564/
no subject
Date: 2022-05-19 10:54 pm (UTC)A thorough local investigation, conducted by the Department of Health in collaboration with eight other government agencies, then indicated that environmental factors had played an important part in this outbreak. Each block at Amoy Gardens has 8 vertical soil stacks collecting effluent from the equivalent section on all floors. The soil stack is connected to the water closets, the basins, the bathtubs and the bathroom floor drains. Each of these sanitary fixtures is fitted with a U-shaped water trap to prevent foul smells and insects getting into the toilets from the soil stack. Clearly, for this to work, the U-traps must contain water. However, because most households were in the habit of cleaning the bathroom floor by mopping rather than flushing with water, the U-traps connected to most floor drains were probably dry and not functioning properly (Figure 2).
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Laboratory studies indicate that many patients with SARS excrete coronavirus in their stools.5 As many as two-thirds of the patients in the Amoy Gardens outbreak had diarrhoea, so a very substantial virus load would have been discharged into the sewerage in Block E. Probably the index patient infected only a small group of Block E residents, with the remainder acquiring the disease via sewage, person-to-person contact and shared communal facilities such as lifts and staircases. These residents subsequently transmitted the disease to others both within and outside Block E through person-to-person contact and environmental contamination.
The bathroom floor drains with dried-up U-traps provided a pathway through which residents came into contact with small droplets containing viruses from the contaminated sewage. These droplets entered the bathroom floor drain through negative pressure generated by exhaust fans when the bathroom was being used with the door closed. Water vapour generated during a shower, and the moist conditions of the bathroom, could also have facilitated the formation of water droplets. The likelihood of exposure was enhanced by the small dimensions of the bathroom units (about 3.5 square metres). Virus-contaminated droplets could readily have been deposited on floor mats, towels, toiletries and other bathroom equipment.
The possibility of disease transmission by other routes—airborne, water-borne, infected dust aerosols—has been examined but there is neither epidemiological nor laboratory support for such mechanisms. A team of environmental experts from the WHO, visiting Amoy Gardens by invitation, agreed with the results of the investigation and also declared the buildings, now cleansed and disinfected, safe for habitation.6