Antigenicity analysis of human parvovirus B19-VP1u protein in the induction of anti-phospholipid syndrome

Lin, Chun Yu; Chiu, Chun Ching; Cheng, Ju Chien; Lin, Chia Yun; Shi, Ya Fang; Tsai, Chun Chou; Tzang, Bor‐Show; Hsu, Tsai‐Ching

doi:10.1080/21505594.2017.1385691

Cited by 14 publications

(10 citation statements)

References 40 publications

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“…Most viral proteins are involved in inflammatory and autoimmune disorders: VP-1, which includes a “VP-1 unique region” (VP-1u) characterized by a phospholipase A2-like activity, probably playing a role in viral entry into the cell [ 108 ] and the generation of inflammatory mediators (leukotrienes and prostaglandins) and phospholipids epitopes, potentially triggering antiphospholipid (aPL) antibodies [ 109 ]. Of note is the fact that VP1-unique region contains many epitopes recognized by neutralizing antibodies, which determine life-long protection [ 106 ].…”

Section: Role Of Specific Viral Infections In Slementioning

confidence: 99%

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Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Quaglia

Merlotti

Andrea

et al. 2021

Viruses

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A causal link between viral infections and autoimmunity has been studied for a long time and the role of some viruses in the induction or exacerbation of systemic lupus erythematosus (SLE) in genetically predisposed patients has been proved. The strength of the association between different viral agents and SLE is variable. Epstein–Barr virus (EBV), parvovirus B19 (B19V), and human endogenous retroviruses (HERVs) are involved in SLE pathogenesis, whereas other viruses such as Cytomegalovirus (CMV) probably play a less prominent role. However, the mechanisms of viral–host interactions and the impact of viruses on disease course have yet to be elucidated. In addition to classical mechanisms of viral-triggered autoimmunity, such as molecular mimicry and epitope spreading, there has been a growing appreciation of the role of direct activation of innate response by viral nucleic acids and epigenetic modulation of interferon-related immune response. The latter is especially important for HERVs, which may represent the molecular link between environmental triggers and critical immune genes. Virus-specific proteins modulating interaction with the host immune system have been characterized especially for Epstein–Barr virus and explain immune evasion, persistent infection and self-reactive B-cell “immortalization”. Knowledge has also been expanding on key viral proteins of B19-V and CMV and their possible association with specific phenotypes such as antiphospholipid syndrome. This progress may pave the way to new therapeutic perspectives, including the use of known or new antiviral drugs, postviral immune response modulation and innate immunity inhibition. We herein describe the state-of-the-art knowledge on the role of viral infections in SLE, with a focus on their mechanisms of action and potential therapeutic targets.

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Section: Role Of Specific Viral Infections In Slementioning

confidence: 99%

“…These patients also had a higher titer of IgG antibodies to B19V compared to those without APS, suggesting a link between previous viral exposure and APS [ 42 ]. The role of protein VP1u as an antigen triggering APS-like syndromes has been established [ 109 ].…”

Section: Role Of Specific Viral Infections In Slementioning

confidence: 99%

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Quaglia

Merlotti

Andrea

et al. 2021

Viruses

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“…The VP1-unique (VP1u) regions of both B19V and HBoV have been shown to exhibit PLA2-like activity and are known to play essential roles in viral infectivity [36–37]. Moreover, the PLA2-like activity of B19V-VP1u and HBoV-VP1u has been implicated in a wide range of pathogenic responses, such as autoimmune diseases, cardiovascular disorders and respiratory diseases [7, 9–10, 38–40]. Our recent studies revealed a disruptive effect of both HBoV-VP1u and B19-VP1u on tight junctions in A549 cells [7] and demonstrated the induction of lung injury by both B19V-VP1u and HBoV-VP1u in naïve mice through the differential regulation of the NF-κB and MAPK signaling pathways [14].…”

Section: Discussionmentioning

confidence: 99%

The effects of human parvovirus VP1 unique region in a mouse model of allergic asthma

et al. 2019

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Evidence has indicated that viral infection increases the risk of developing asthma. Although the association of human parvovirus B19 (B19V) or human bocavirus (HBoV) with respiratory diseases has been reported, little is known about the influence of the B19V-VP1u and HBoV-VP1u proteins on the symptoms of asthma. Herein, we investigated the systemic influence of subcutaneously injected B19V-VP1u and HBoV-VP1u recombinant proteins in an OVA-sensitized asthmatic mouse model. A significantly higher Penh ratio and IgE level were detected in the serum, bronchoalveolar lavage fluid (BALF) and the supernatant of a lymphocyte culture from mice treated with HBoV-VP1u or B19V-VP1u than in a lymphocyte culture from OVA-sensitized mice. Significantly higher levels of serum and BALF IgE, total IgG, IgG1, OVA-specific IgE and OVA-specific IgG1 were detected in mice treated with HBoV-VP1u or B19V-VP1u than in OVA-sensitized mice. Conversely, a significantly lower IgG2a level was detected in mice from the HBoV-VP1u or B19V-VP1u groups than in mice from the OVA group. The mice treated with HBoV-VP1u or B19V-VP1u exhibited more significant lung inflammatory indices, including elevated serum and BALF IL-4, IL-5, IL-10 and IL-13 levels; BALF lymphocyte, neutrophil and eosinophil counts, MMP-9 and MMP-2 activity; and the amount of lymphocyte infiltration, relative to those in the control mice or in those sensitized with OVA. These findings demonstrate that the subcutaneous injection of HBoV-VP1u or B19V-VP1u proteins in OVA-sensitized mice result in elevated asthmatic indices and suggest that human parvoviruses may increase the risk of developing airway inflammation in a mouse model of asthma.

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“…The sPLA2-like activity of B19V-VP1u and HBoV-VP1u has also been linked to a wide range of pathogenic responses, including autoimmune disorders, cardiovascular disorders and respiratory infection [ 17 , 48 ]. Indeed, evidence has indicated that the unique region of VP1 in B19V and HBoV plays a crucial role in infection and induce inflammation in host cells or tissues due to its phospholipase A2 (PLA2)-like activity [ 14 – 16 , 48 – 50 ]. Although previous studies have reported that B19-VP1u protein induces myocardial inflammation and liver injury in naïve mice [ 48 – 49 ], little is known whether HBoV-VP1u affect the other organs in mice receiving HBoV-VP1u protein.…”

Section: Discussionmentioning

confidence: 99%

The VP1 unique region of human parvovirus B19 and human bocavirus induce lung injury in naïve Balb/c mice

et al. 2018

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Both human parvovirus B19 (B19V) and human bocavirus (HBoV) are known to be important human pathogens of the Parvoviridae family. Our earlier investigation demonstrated that both B19V-VP1u and HBoV-VP1u have a significantly disruptive effect on tight junctions (TJs) in A549 cells, implying the essential role of parvovirus in airway infection and lung injury. However, no direct evidence that B19V-VP1u and HBoV-VP1u induce lung injury exists. The present study further investigates the induction of lung injury by B19V-VP1u and HBoV-VP1u in naïve Balb/c mice following subcutaneous injection of PBS, recombinant B19V-VP1u or HBoV-VP1u. The experimental results reveal significantly increased activity, protein expression and ratio of matrix metalloproteinase-9 (MMP-9) to MMP-2 in Balb/c mice that received B19V-VP1u or HBoV-VP1u compared to those that received PBS. Significantly higher levels of inflammatory cytokines, including IL-6 and IL-1β, and greater lymphocyte infiltration in lung tissue sections were detected in mice that received B19V-VP1u or HBoV-VP1u. Additionally, significantly increased levels of phosphorylated p65 (NF-κB) and MAPK signaling proteins were observed in lung tissue of mice that received B19V-VP1u or HBoV-VP1u compared to those of mice that received PBS. These findings demonstrate for the first time that B19V-VP1u and HBoV-VP1u proteins induce lung inflammatory reactions through p65 (NF-κB) and MAPK signaling.

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Antigenicity analysis of human parvovirus B19-VP1u protein in the induction of anti-phospholipid syndrome

Cited by 14 publications

References 40 publications

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

The effects of human parvovirus VP1 unique region in a mouse model of allergic asthma

The VP1 unique region of human parvovirus B19 and human bocavirus induce lung injury in naïve Balb/c mice

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