Homotypic immune response to primary infection with rotavirus serotype G1

1995 ◽  
Vol 47 (4) ◽  
pp. 404-409 ◽  
Author(s):  
A. M. Rojas ◽  
Y. Boher ◽  
M. J. Guntinas ◽  
I. Pérez-Schael
2021 ◽  
Author(s):  
Lotus Leonie van den Hoogen ◽  
Gaby Smits ◽  
Cheyenne CE van Hagen ◽  
Denise Wong ◽  
Eric RA Vos ◽  
...  

Background With COVID-19 vaccine roll-out ongoing in many countries globally, monitoring of breakthrough infections is of great importance. Antibodies persist in the blood after a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Since COVID-19 vaccines induce immune response to the Spike protein of the virus, which is the main serosurveillance target to date, alternative targets should be explored to distinguish infection from vaccination. Methods Multiplex immunoassay data from 1,513 SARS-CoV-2 RT-qPCR-tested individuals (352 positive and 1,161 negative) with a primary infection and no vaccination history were used to determine the accuracy of Nucleoprotein-specific immunoglobulin G (IgG) in detecting past SARS-CoV-2 infection. We also described Spike S1 and Nucleoprotein-specific IgG responses in 230 COVID-19 vaccinated individuals (Pfizer/BioNTech). Results The sensitivity of Nucleoprotein seropositivity was 85% (95% confidence interval: 80-90%) for mild COVID-19 in the first two months following symptom onset. Sensitivity was lower in asymptomatic individuals (67%, 50-81%). Participants who had experienced a SARS-CoV-2 infection up to 11 months preceding vaccination, as assessed by Spike S1 seropositivity or RT-qPCR, produced 2.7-fold higher median levels of IgG to Spike S1 ≥14 days after the first dose as compared to those unexposed to SARS-CoV-2 at ≥7 days after the second dose (p=0.011). Nucleoprotein-specific IgG concentrations were not affected by vaccination in naïve participants. Conclusions Serological responses to Nucleoprotein may prove helpful in identifying SARS-CoV-2 infections after vaccination. Furthermore, it can help interpret IgG to Spike S1 after COVID-19 vaccination as particularly high responses shortly after vaccination could be explained by prior exposure history.


2020 ◽  
Author(s):  
Jianmin Zuo ◽  
Alex Dowell ◽  
Hayden Pearce ◽  
Kriti Verma ◽  
Heather Long ◽  
...  

Abstract The immune response to SARS-CoV-2 is critical in both controlling primary infection and preventing re-infection. However, there is concern that immune responses following natural infection may not be sustained and that this may predispose to recurrent infection. We analysed the magnitude and phenotype of the SARS-CoV-2 cellular immune response in 100 donors at six months following primary infection and related this to the profile of antibody level against spike, nucleoprotein and RBD over the previous six months. T-cell immune responses to SARS-CoV-2 were present by ELISPOT or ICS analysis in all donors and are characterised by predominant CD4+ T cell responses with strong IL-2 cytokine expression. Median T-cell responses were 50% higher in donors who had experienced an initial symptomatic infection indicating that the severity of primary infection establishes a ‘setpoint’ for cellular immunity that lasts for at least 6 months. The T-cell responses to both spike and nucleoprotein/membrane proteins were strongly correlated with the peak antibody level against each protein. The rate of decline in antibody level varied between individuals and higher levels of nucleoprotein-specific T cells were associated with preservation of NP-specific antibody level although no such correlation was observed in relation to spike-specific responses. In conclusion, our data are reassuring that functional SARS-CoV-2-specific T-cell responses are retained at six months following infection although the magnitude of this response is related to the clinical features of primary infection.


Parasitology ◽  
1989 ◽  
Vol 98 (2) ◽  
pp. 301-306
Author(s):  
Lucy J. Robertson

SUMMARYThe activity of the gluconeogenic enzyme, alanine-amino-transferase (ALT), in a preparation from the liver of rats was studied by means of an in vitro assay throughout the course of a primary infection of Nippostrongylus brasiliensis, established by a subcutaneous injection of approximately 4000 3rd-stage larvae. The activity was measured on days 1–14 p.i. in both uninfected and infected rats and a marked pattern in the enzyme's activity was observed. In infected rats, the activity increased from 1·46±0·19 U/g liver on day 1 p.i. to a peak on day 4 p.i. of 10·75±1·62 U/g liver, then decreased to a trough of 0·44±0·18 U/g liver on day 10 p.i. before returning to original levels by day 14 p.i., by which time the infection had been largely eliminated. In uninfected rats the activity of the liver enzyme remained constant throughout this period with a value of 2·54±0·12 U/g liver. The activity of the enzyme in vitro was found to be related to the size of the inoculum on days 4 and 10 p.i. It was proposed that these observations could be due to either (1) a direct effect of the parasite, or (2) a consequence of the host immune response to the infection. In order to investigate the second proposition more fully, liver ALT activity was investigated by in vitro assay on selected days p.i. in rats experiencing a secondary N. brasiliensis infection. In these rats the liver ALT activity was observed to reach a peak on day 2 p.i., with an activity of 3·87 ± 0-28 U/g liver, and a trough on day 4 p.i. with an activity of 0·11 ±0·03 U/g liver, returning to similar levels to those measured in uninfected rats by day 7 p.i. When serum prepared from rats having secondary N. brasiliensis infections collected on day 4 p.i. was added to the assay, a reduction in the activity of liver ALT activity from both the infected and uninfected rats was measured by in vitro assay. The results are discussed in relation to protein metabolism and gluconeogenesis in rats infected with N. brasiliensis, and also in relation to the host’s immune response to the parasitic infection.


Author(s):  
Graham Cooke

Sepsis is a clinical syndrome defined by the presence of both infection and a systemic inflammatory response with or without organ damage. The pathogenesis of sepsis is complex and may differ according to the infecting microbe, the site of primary infection, and the host’s immunological and physiological status prior to infection. The term ‘systemic inflammatory response syndrome’ refers to the clinical manifestations of a dysregulated host immune response, while ‘bacteraemia’, in contrast, refers to the presence of viable organisms that can be cultured from blood.


2010 ◽  
Vol 18 (4) ◽  
pp. 385-399 ◽  
Author(s):  
Prashant K. Srivastava ◽  
M. Banerjee ◽  
Peeyush Chandra

Author(s):  
Ahmed Babiker ◽  
Charles Marvil ◽  
Jesse J. Waggoner ◽  
Matthew Collins ◽  
Anne Piantadosi

Reports of SARS-CoV-2 reinfection have raised important questions about the strength and durability of the immune response to primary infection, which are key factors in predicting the course of the pandemic. Identifying reinfection requires detecting the virus at two different time points and using viral genomic data to distinguish reinfection from persistent viral carriage. This process is hindered by challenges of logistics and capacity, such as banking samples from primary infection and performing viral genome sequencing. These challenges may help to explain why very few cases have been described to date. In addition, reinfection may be a rare phenomenon, but detailed prospective studies are needed to rigorously assess its frequency. To provide context for future investigations of SARS-CoV-2 reinfection, we review 16 cases that have been published to date or are available in pre-print. Reinfection occurred across demographic spectra and in patients whose initial infections were both asymptomatic/mild and moderate/severe. For cases in which severity could be compared between episodes, half of reinfections were less severe, raising the possibility of partial immune protection. Although many patients had a positive total immunoglobulin or IgG result at the time of reinfection, very little examination of their immune response was performed. Further work is needed to elucidate the frequency, determinants, and consequences of SARS-CoV-2 reinfection. Establishing the necessary frameworks for surveillance and investigation will rely heavily on clinical laboratories and clinical investigators, and we propose several considerations to guide the medical community in identifying and characterizing SARS-CoV-2 reinfections.


2020 ◽  
Vol 4 (4) ◽  
pp. 353-356
Author(s):  
Kyle R Bhatia ◽  
Robert T Brodell ◽  
Ashish C Bhatia ◽  
Chelsea S Mockbee

Infectious eczematoid dermatitis (IED) is defined as an acute, eczematous eruption that occurs secondary to autosensitization to purulent drainage from a primary infected site. The condition is believed to develop when bacterial products, most often the result of Staphylococcal or Streptococcal species, act as haptens and stimulate an immune response. IED typically manifests as a plaque with associated vesicles and pustules surrounding drainage from a central infectious source, or as oozing, erythema, crusting, and scaling spreading peripherally from a central infectious source. Management of IED includes both targeting the causative primary infection and suppressing the immune response producing a hypersensitivity reaction. This report details two cases. Case 1 describes a common presentation of tinea pedis. Case 2 is that of a 28 year-old-male who presented with an acute onset tender, pruritic, weeping rash after wearing boots for two straight days, and who was subsequently diagnosed and treated for IED.


Parasitology ◽  
1974 ◽  
Vol 68 (1) ◽  
pp. 13-17 ◽  
Author(s):  
D. Conwil Jenkins

Previously immunized rats of different ages were exposed either to one large, or several small challenge infections with the nematode, Nippostrongylus brasiliensis. The number of secondary worms harboured by each of these rats was then determined on the fourteenth day after exposure to challenge. It was found that worms adapted more efficiently to host immunity when both (a) the rats were less than 11 weeks old when challenged and (b) the challenge was given in small repeated doses over a period of weeks. The age of the rats on exposure to the immunizing primary infection, however, had little or no affect per se on the subsequent establishment of immune-adapted worms. It is tentatively suggested that the failure of worms to adapt effectively to the acquired immunity of older rats resulted from the acquisition by these rats of a fully competent cellular immune response.


2012 ◽  
Vol 80 (3) ◽  
pp. 943-951 ◽  
Author(s):  
Duangjit Kanistanon ◽  
Daniel A. Powell ◽  
Adeline M. Hajjar ◽  
Mark R. Pelletier ◽  
Ilana E. Cohen ◽  
...  

Lipopolysaccharide (LPS) structural modifications have been shown to specifically affect the pathogenesis of many Gram-negative pathogens. InFrancisella, modification of the lipid A component of LPS resulted in a molecule with no to low endotoxic activity. The role of the terminal lipid A phosphates in host recognition and pathogenesis was determined using aFrancisella novicidamutant that lacked the 4′ phosphatase enzyme (LpxF). The lipid A of this strain retained the phosphate moiety at the 4′ position and the N-linked fatty acid at the 3′ position on the diglucosamine backbone. Studies were undertaken to determine the pathogenesis of this mutant strain via the pulmonary and subcutaneous routes of infection. Mice infected with thelpxF-nullF. novicidamutant by either route survived primary infection and subsequently developed protective immunity against a lethal wild-type (WT)F. novicidachallenge. To determine the mechanism(s) by which the host controlled primary infection by thelpxF-null mutant, the role of innate immune components, including Toll-like receptor 2 (TLR2), TLR4, caspase-1, MyD88, alpha interferon (IFN-α), and gamma interferon(IFN-γ), was examined using knockout mice. Interestingly, only the IFN-γ knockout mice succumbed to a primarylpxF-nullF. novicidamutant infection, highlighting the importance of IFN-γ production. To determine the role of components of the host adaptive immune system that elicit the long-term protective immune response, T- and B-cell deficient RAG1−/−mice were examined. All mice survived primary infection; however, RAG1−/−mice did not survive WT challenge, highlighting a role for T and B cells in the protective immune response.


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