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PloS One 2021The recovery of other pathogens in patients with SARS-CoV-2 infection has been reported, either at the time of a SARS-CoV-2 infection diagnosis (co-infection) or... (Meta-Analysis)
Meta-Analysis
INTRODUCTION
The recovery of other pathogens in patients with SARS-CoV-2 infection has been reported, either at the time of a SARS-CoV-2 infection diagnosis (co-infection) or subsequently (superinfection). However, data on the prevalence, microbiology, and outcomes of co-infection and superinfection are limited. The purpose of this study was to examine the occurrence of co-infections and superinfections and their outcomes among patients with SARS-CoV-2 infection.
PATIENTS AND METHODS
We searched literature databases for studies published from October 1, 2019, through February 8, 2021. We included studies that reported clinical features and outcomes of co-infection or superinfection of SARS-CoV-2 and other pathogens in hospitalized and non-hospitalized patients. We followed PRISMA guidelines, and we registered the protocol with PROSPERO as: CRD42020189763.
RESULTS
Of 6639 articles screened, 118 were included in the random effects meta-analysis. The pooled prevalence of co-infection was 19% (95% confidence interval [CI]: 14%-25%, I2 = 98%) and that of superinfection was 24% (95% CI: 19%-30%). Pooled prevalence of pathogen type stratified by co- or superinfection were: viral co-infections, 10% (95% CI: 6%-14%); viral superinfections, 4% (95% CI: 0%-10%); bacterial co-infections, 8% (95% CI: 5%-11%); bacterial superinfections, 20% (95% CI: 13%-28%); fungal co-infections, 4% (95% CI: 2%-7%); and fungal superinfections, 8% (95% CI: 4%-13%). Patients with a co-infection or superinfection had higher odds of dying than those who only had SARS-CoV-2 infection (odds ratio = 3.31, 95% CI: 1.82-5.99). Compared to those with co-infections, patients with superinfections had a higher prevalence of mechanical ventilation (45% [95% CI: 33%-58%] vs. 10% [95% CI: 5%-16%]), but patients with co-infections had a greater average length of hospital stay than those with superinfections (mean = 29.0 days, standard deviation [SD] = 6.7 vs. mean = 16 days, SD = 6.2, respectively).
CONCLUSIONS
Our study showed that as many as 19% of patients with COVID-19 have co-infections and 24% have superinfections. The presence of either co-infection or superinfection was associated with poor outcomes, including increased mortality. Our findings support the need for diagnostic testing to identify and treat co-occurring respiratory infections among patients with SARS-CoV-2 infection.
Topics: Bacterial Infections; COVID-19; Coinfection; Hospitalization; Humans; Mycoses; Prevalence; SARS-CoV-2; Superinfection; Treatment Outcome; Virus Diseases
PubMed: 33956882
DOI: 10.1371/journal.pone.0251170 -
Current Opinion in Infectious Diseases Feb 2012This review describes the nature and frequency of HIV-1 superinfection and provides advice regarding counselling of patients in accordance with national guidelines. (Review)
Review
PURPOSE OF REVIEW
This review describes the nature and frequency of HIV-1 superinfection and provides advice regarding counselling of patients in accordance with national guidelines.
RECENT FINDINGS
Recent studies have demonstrated conflicting results, from no superinfection to an incidence of over 18%. We discuss the difficulties comparing studies due to population and methodological differences.
SUMMARY
HIV-infected individuals should be counselled that there is risk of superinfection at all stages of HIV, but this is unlikely to be clinically significant unless transmission of resistance occurs. The risk may be as high as the risk of new incident infection in the presence of on-going exposure.
Topics: Counseling; HIV Infections; HIV-1; Humans; Incidence; Practice Guidelines as Topic; Species Specificity; Superinfection
PubMed: 22156898
DOI: 10.1097/QCO.0b013e32834ef5af -
PLoS Computational Biology May 2022Viral superinfection occurs when multiple viral particles subsequently infect the same host. In nature, several viral species are found to have evolved diverse...
Viral superinfection occurs when multiple viral particles subsequently infect the same host. In nature, several viral species are found to have evolved diverse mechanisms to prevent superinfection (superinfection exclusion) but how this strategic choice impacts the fate of mutations in the viral population remains unclear. Using stochastic simulations, we find that genetic drift is suppressed when superinfection occurs, thus facilitating the fixation of beneficial mutations and the removal of deleterious ones. Interestingly, we also find that the competitive (dis)advantage associated with variations in life history parameters is not necessarily captured by the viral growth rate for either infection strategy. Putting these together, we then show that a mutant with superinfection exclusion will easily overtake a superinfecting population even if the latter has a much higher growth rate. Our findings suggest that while superinfection exclusion can negatively impact the long-term adaptation of a viral population, in the short-term it is ultimately a winning strategy.
Topics: Humans; Superinfection
PubMed: 35536864
DOI: 10.1371/journal.pcbi.1010125 -
Frontiers in Immunology 2019Despite the widespread application of vaccination programs and antiviral drug treatments, influenza viruses are still among the most harmful human pathogens. Indeed,... (Review)
Review
Despite the widespread application of vaccination programs and antiviral drug treatments, influenza viruses are still among the most harmful human pathogens. Indeed, influenza results in significant seasonal and pandemic morbidity and mortality. Furthermore, severe bacterial infections can occur in the aftermath of influenza virus infection, and contribute substantially to the excess morbidity and mortality associated with influenza. Here, we review the main features of influenza viruses and current knowledge about the mechanical and immune mechanisms that underlie post-influenza secondary bacterial infections. We present the emerging literature describing the role of "innate-like" unconventional T cells in post-influenza bacterial superinfection. Unconventional T cell populations span the border between the innate and adaptive arms of the immune system, and are prevalent in mucosal tissues (including the airways). They mainly comprise Natural Killer T cells, mucosal-associated invariant T cells and γδ T cells. We provide an overview of the principal functions that these cells play in pulmonary barrier functions and immunity, highlighting their unique ability to sense environmental factors and promote protection against respiratory bacterial infections. We focus on two major opportunistic pathogens involved in superinfections, namely and . We discuss mechanisms through which influenza viruses alter the antibacterial activity of unconventional T cells. Lastly, we discuss recent fundamental advances and possible therapeutic approaches in which unconventional T cells would be targeted to prevent post-influenza bacterial superinfections.
Topics: Animals; Bacterial Infections; Humans; Influenza, Human; Superinfection; T-Lymphocytes
PubMed: 30881357
DOI: 10.3389/fimmu.2019.00336 -
EMBO Reports Dec 2011After the bite of a malaria-infected mosquito, the Plasmodium sporozoite infects liver cells and produces thousands of merozoites, which then infect red blood cells,... (Review)
Review
After the bite of a malaria-infected mosquito, the Plasmodium sporozoite infects liver cells and produces thousands of merozoites, which then infect red blood cells, causing malaria. In malaria-endemic areas, several hundred infected mosquitoes can bite an individual each year, increasing the risk of superinfection. However, in infants that are yet to acquire immunity, superinfections are infrequent. We have recently shown that blood-stage parasitaemia, above a minimum threshold, impairs the growth of a subsequent sporozoite infection of liver cells. Blood-stage parasites stimulate the production of the host iron-regulatory factor hepcidin, which redistributes iron away from hepatocytes, reducing the development of the iron-dependent liver stage. This could explain why Plasmodium superinfection is not often found in young nonimmune children. Here, we discuss the impact that such protection from superinfection might have in epidemiological settings or in programmes for controlling malaria, as well as how the induction of hepcidin and redistribution of iron might influence anaemia and the outcome of non-Plasmodium co-infections.
Topics: Host-Parasite Interactions; Humans; Immunity; Iron; Malaria; Plasmodium; Superinfection
PubMed: 22081142
DOI: 10.1038/embor.2011.213 -
The Lancet. Microbe Jul 2020
Topics: COVID-19; Humans; Pulmonary Aspergillosis; Superinfection
PubMed: 32835341
DOI: 10.1016/S2666-5247(20)30065-3 -
Antiviral Therapy 2012The majority of acute HCV infections progress to chronicity, implying that the immune response is unable to clear virus in most instances. Reinfection with a second... (Review)
Review
The majority of acute HCV infections progress to chronicity, implying that the immune response is unable to clear virus in most instances. Reinfection with a second strain of HCV after clearance of an initial infection has been reported in several recent studies. Moreover, individuals with HCV infection may be at risk of HCV superinfection with a second strain of HCV even after the establishment of persistent infection and the development of an immunological response to the initial virus. In vivo and in vitro data regarding HCV reinfection and superinfection, including the clinical consequences of these phenomena and the impact they have on vaccines require consideration in future studies.
Topics: Hepacivirus; Hepatitis C; Humans; Recombination, Genetic; Recurrence; Superinfection
PubMed: 23221168
DOI: 10.3851/IMP2460 -
Annual Review of Virology Sep 2022Natural selection acts on cellular organisms by ensuring the genes responsible for an advantageous phenotype consistently reap the phenotypic advantage. This is possible... (Review)
Review
Natural selection acts on cellular organisms by ensuring the genes responsible for an advantageous phenotype consistently reap the phenotypic advantage. This is possible because reproductive cells of these organisms are almost always haploid, separating the beneficial gene from its rival allele at every generation. How natural selection acts on plus-strand RNA viruses is unclear because these viruses frequently load host cells with numerous genome copies and replicate thousands of progeny genomes in each cell. Recent studies suggest that these viruses encode the Bottleneck, Isolate, Amplify, Select (BIAS) mechanism that blocks all but a few viral genome copies from replication, thus creating the environment in which the bottleneck-escaping viral genome copies are isolated from each other, allowing natural selection to reward beneficial mutations and purge lethal errors. This BIAS mechanism also blocks the genomes of highly homologous superinfecting viruses, thus explaining cellular-level superinfection exclusion.
Topics: Cell Line; Genome, Viral; Humans; RNA Viruses; Selection, Genetic; Superinfection; Virus Replication
PubMed: 35567296
DOI: 10.1146/annurev-virology-100520-114758 -
Current HIV Research Jul 2004Superinfection is defined as infection by a second virus during an immunologic steady state, following infection by a primary virus. It is now well established that... (Review)
Review
Superinfection is defined as infection by a second virus during an immunologic steady state, following infection by a primary virus. It is now well established that superinfection with HIV-1 occurs in humans. Detection of an increasing number of circulating recombinant forms, which result from infection of a cell by two or more clades, suggests that superinfection occurs more frequently than previously thought. The second virus (from a different clade or the same clade as the primary virus) can superinfect some time after the first and this is associated with rapid viral rebound and immune decline. Primary infection with a specific clade appears not to provide cross-protection against superinfection with a different clade or the same clade. Estimating the overall impact of HIV-1 superinfection on pathogenesis and attempts to create a broadly protective prophylactic HIV-1 vaccine is complicated by our inability to quantify the true incidence and prevalence.
Topics: Animals; HIV Infections; HIV-1; Humans; Recombination, Genetic; Superinfection
PubMed: 15279590
DOI: 10.2174/1570162043351219 -
Archives of Oral Biology Apr 2016Peri-implantitis has emerged in the last few years as a complication difficult to resolve. The etiopathogenesis consensus is mainly attributed to bacteria. Following the... (Review)
Review
Peri-implantitis has emerged in the last few years as a complication difficult to resolve. The etiopathogenesis consensus is mainly attributed to bacteria. Following the preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines, a PubMed/Medline literature search was performed using the US National Library of Medicine database up to 2015 to analyze available scientific data on the rationale and risk of superinfection associated to systemic antimicrobials in human peri-implant disease. A hand search was also conducted on relevant medical and microbiology journals. The methodological index for non-randomized studies (MINORS) was independently assessed for quality on the selected papers. Proposed combined therapies use broad-spectrum antibiotics to halt the disease progression. A major associated risk, particularly when prescribed empirically without microbiological follow-up, is the undetected development of superinfections and overgrowth of opportunistic pathogens difficult to eradicate. Peri-implant superinfections with opportunistic bacteria, yeast and viruses, are plausible risks associated to the use of systemic antibiotics in immunocompetent individuals. Lack of microbiological follow-up and antibiotic susceptibility testing may lead to ongoing microbial challenges that exacerbate the disease progression. The increased proliferation of antimicrobial resistance, modern implant surface topography and indiscriminative empiric antibiotic regimens may promote the escalation of peri-implant disease in years to come. A personalized 3-month supportive therapy may help prevent risks by sustaining a normal ecological balance, decreasing specific pathogen proportions and maintaining ideal plaque control.
Topics: Anti-Bacterial Agents; Biofilms; Dental Implants; Dental Plaque; Drug Resistance, Microbial; Humans; Opportunistic Infections; Peri-Implantitis; Superinfection; United States
PubMed: 26761363
DOI: 10.1016/j.archoralbio.2015.12.007