| 1. |
|
|
| 2. |
|
|
| 3. |
- Fridholm, Helena, et al.
(författare)
-
Immunogenicity properties of authentic and heterologously synthesized structural protein VP2 of infectious pancreatic necrosis virus.
- 2007
-
Ingår i: Viral Immunology. - : Mary Ann Liebert Inc. - 0882-8245 .- 1557-8976. ; 20:4, s. 635-648
-
Tidskriftsartikel (refereegranskat)abstract
- The sole coat protein VP2 of infectious pancreatic necrosis virus (IPNV) was isolated and purified from intact virions, propagated in CHSE-214 cells. Likewise was the full-length VP2 protein isolated and purified upon cloning and expression of the corresponding complete gene in E. coli. The two purified proteins of different synthetic origins carrying identical primary structures were utilized in an immunization program using a rabbit model. Sera obtained against both immunogens react equally well with authentic and recombinant VP2 in Western blots and ELISAs. Also, the total net binding forces as determined by avidity index (AI) calculations were high and of similar stature, exceeding 80. An IPNV infection of susceptible and permissive CHSE-214 cells could only be neutralized by IgG preparations obtained from rabbits immunized with authentic VP2. Only such antibodies were able to aggregate and sediment radiolabeled virions in glycerol gradients upon rate zonal centrifugations. The presence of sugar moieties on the authentic protein is suggested to be of pivotal importance in eliciting an immune response capable of preventing infection in cell cultures in vitro.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Hurwitz, Julia L., et al.
(författare)
-
Hypothesis : RNA and DNA Viral Sequence Integration into the Mammalian Host Genome Supports Long-Term B Cell and T Cell Adaptive Immunity
- 2017
-
Ingår i: Viral immunology. - : MARY ANN LIEBERT, INC. - 0882-8245 .- 1557-8976. ; 30:9, s. 628-632
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Viral sequence integration into the mammalian genome has long been perceived as a health risk. In some cases, integration translates to chronic viral infection, and in other instances, oncogenic gene mutations occur. However, research also shows that animal cells can benefit from integrated viral sequences (e.g., to support host cell development or to silence foreign invaders). Here we propose that, comparable with the clustered regularly interspaced short palindromic repeats that provide bacteria with adaptive immunity against invasive bacteriophages, animal cells may co-opt integrated viral sequences to support immune memory. We hypothesize that host cells express viral peptides from open reading frames in integrated sequences to boost adaptive B cell and T cell responses long after replicating viruses are cleared. In support of this hypothesis, we examine previous literature describing (1) viruses that infect acutely (e.g., vaccinia viruses and orthomyxoviruses) followed by unexplained, long-term persistence of viral nucleotide sequences, viral peptides, and virus-specific adaptive immunity, (2) the high frequency of endogenous viral genetic elements found in animal genomes, and (3) mechanisms with which animal host machinery supports foreign sequence integration.
|
|
| 7. |
- Johansson, Susanne E, et al.
(författare)
-
NK Cell Function and Antibodies Mediating ADCC in HIV-1-Infected Viremic and Controller Patients
- 2011
-
Ingår i: Viral immunology. - : Mary Ann Liebert. - 0882-8245 .- 1557-8976. ; 24:5, s. 359-368
-
Tidskriftsartikel (refereegranskat)abstract
- Natural killer (NK) cells have been suggested to play a protective role in HIV disease progression. One potent effector mechanism of NK cells is antibody-dependent cellular cytotoxicity (ADCC) mediated by antiviral antibodies binding to the Fc gamma RIIIa receptor (CD16) on NK cells. We investigated NK cell-mediated ADCC function and the presence of ADCC antibodies in plasma from 20 HIV-1-infected patients and 10 healthy donors. The HIV-positive patients were divided into two groups: six who controlled viremia for at least 8 y without treatment (controllers), and 14 who were persistently viremic and not currently on treatment. Plasma from both patient groups induced NK cell IFN-gamma expression and degranulation in response to HIV-1 envelope (Env) gp140-protein-coated cells. Patient antibodies mediating ADCC were largely directed towards the Env V3 loop, as identified by a gp140 protein lacking the V3 loop. Interestingly, in two controllers ADCC-mediating antibodies were more broadly directed to other parts of Env. A high viral load in patients correlated with decreased ADCC-mediated cytolysis of gp140-protein-coated target cells. NK cells from both infected patients and healthy donors degranulated efficiently in the presence of antibody-coated HIV-1-infected Jurkat cells. In conclusion, the character of ADCC-mediating antibodies differed in some controllers compared to viremic patients. NK cell ADCC activity is not compromised in HIV-infected patients.
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Lind, Alexander, et al.
(författare)
-
Antibody Affinity Against 2009 A/H1N1 Influenza and Pandemrix Vaccine Nucleoproteins Differs Between Childhood Narcolepsy Patients and Controls
- 2017
-
Ingår i: Viral immunology. - : Mary Ann Liebert Inc. - 0882-8245 .- 1557-8976. ; 30:8, s. 590-600
-
Tidskriftsartikel (refereegranskat)abstract
- Increased narcolepsy incidence was observed in Sweden following the 2009 influenza vaccination with Pandemrix((R)). A substitution of the 2009 nucleoprotein for the 1934 variant has been implicated in narcolepsy development. The aims were to determine (a) antibody levels toward wild-type A/H1N1-2009[A/California/04/2009(H1N1)] (NP-CA2009) and Pandemrix-[A/Puerto Rico/8/1934(H1N1)] (NP-PR1934) nucleoproteins in 43 patients and 64 age-matched controls; (b) antibody affinity in reciprocal competitive assays in 11 childhood narcolepsy patients compared with 21 age-matched controls; and (c) antibody levels toward wild-type A/H1N1-2009[A/California/04/2009(H1N1)] (H1N1 NS1), not a component of the Pandemrix vaccine. In vitro transcribed and translated S-35-methionine-labeled H1N1 influenza A virus proteins were used in radiobinding reciprocal competition assays to estimate antibody levels and affinity (Kd). Childhood patients had higher NP-CA2009 (p=0.0339) and NP-PR1934 (p=0.0246) antibody levels compared with age-matched controls. These childhood controls had lower NP-CA2009 (p=0.0221) and NP-PR1934 (p=0.00619) antibodies compared with controls 13 years or older. In contrast, in patients 13 years or older, the levels of NP-PR1934 (p=0.279) and NP-CA2009 (p=0.0644) antibodies did not differ from the older controls. Childhood antibody affinity (Kd) against NP-CA2009 was comparable between controls (68ng/mL) and patients (74ng/mL; p=0.21) with NP-CA2009 and NP-PR1934 displacement (controls: 165ng/mL; patients: 199ng/mL; p=0.48). In contrast, antibody affinity against NP-PR1934 was higher in controls with either NP-PR1934 (controls: 9ng/mL; patients: 20ng/mL; p=0.0031) or NP-CA2009 (controls: 14ng/mL; patients: 23ng/mL; p=0.0048). A/H1N1-NS1 antibodies were detected in 0/43 of the narcolepsy patients compared with 3/64 (4.7%) controls (p=0.272). Similarly, none (0/11) of the childhood patients and 1/21 (4.8%) of the childhood controls had A/H1N1-NS1 antibodies. The higher antibody affinities against NP-PR1934 in controls suggest better protection against wild-type virus. In contrast, the reduced NP-PR1934 antibody affinities among childhood narcolepsy patients suggest poor protection from the wild-type A/H1N1 virus and possibly increased risk for viral damage.
|
|
