2020 taxonomic update for phylum Negarnaviricota (Riboviria: Orthornavirae), including the large orders Bunyavirales and Mononegavirales.

In March 2020, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. At the genus rank, 20 new genera were added, two were deleted, one was moved, and three were renamed. At the species rank, 160 species were added, four were deleted, ten were moved and renamed, and 30 species were renamed. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV

Efficacy of Gamma Interferon and Specific Antibody for Treatment of Microsporidiosis Caused by Encephalitozoon cuniculi in SCID Mice▿

Microsporidia are eukaryotic, obligate, intracellular protists that are emerging pathogens in immunocompromised hosts, including AIDS patients and organ transplant recipients. The efficacy of gamma interferon (IFN-γ) for the treatment of microsporidiosis caused by Encephalitozoon cuniculi was studied by means of adoptive transfer and IFN-γ administration in SCID mice. While the adoptive transfer of CD4+ T cells from immunocompetent mice prolonged survival of SCID mice infected perorally with E. cuniculi, survival was not improved by adoptive transfer of CD4+ T lymphocytes from IFN-γ-deficient mice. The protective effect of IFN-γ was confirmed in cytokine therapy experiments in which SCID mice receiving IFN-γ survived significantly longer than mice receiving mock injections. The administration of serum containing specific antibodies against E. cuniculi was found to prolong the survival of concurrently IFN-γ-treated SCID mice. The data presented in this study suggest that IFN-γ is potentially useful as a cytokine therapy for microsporidiosis, especially in CD4+ T-cell-deficient patients

Breakdown of the blood-brain barrier during tick-borne encephalitis in mice is not dependent on CD8+ T-cells.

Tick-borne encephalitis (TBE) virus causes severe encephalitis with serious sequelae in humans. The disease is characterized by fever and debilitating encephalitis that can progress to chronic illness or fatal infection. In this study, changes in permeability of the blood-brain barrier (BBB) in two susceptible animal models (BALB/c, and C57Bl/6 mice) infected with TBE virus were investigated at various days after infection by measuring fluorescence in brain homogenates after intraperitoneal injection of sodium fluorescein, a compound that is normally excluded from the central nervous system. We demonstrate here that TBE virus infection, in addition to causing fatal encephalitis in mice, induces considerable breakdown of the BBB. The permeability of the BBB increased at later stages of TBE infection when high virus load was present in the brain (i.e., BBB breakdown was not necessary for TBE virus entry into the brain), and at the onset of the first severe clinical symptoms of the disease, which included neurological signs associated with sharp declines in body weight and temperature. The increased BBB permeability was in association with dramatic upregulation of proinflammatory cytokine/chemokine mRNA expression in the brain. Breakdown of the BBB was also observed in mice deficient in CD8(+) T-cells, indicating that these cells are not necessary for the increase in BBB permeability that occurs during TBE. These novel findings are highly relevant to the development of future therapies designed to control this important human infectious disease

Examination of immunogenic properties of recombinant antigens based on p22 protein from African swine fever virus

The single member of the Asfarviridae family is African swine fever virus (ASFV). This double-stranded DNA virus infects wild and farmed swine and loses the pig industry large sums of money. An inner envelope, capsid, and outer envelope are parts of the ASFV particle containing structural proteins playing different roles in the process of infection or host immune defence evasion. When expressed by the baculovirus system, the p22 protein from the inner envelope was found to induce partial protection against a virulent virus strain. This study aimed to express a part of this protein in a different system and evaluate its immunogenicity

Tick-Borne Encephalitis in an 8.5-Month-Old Boy Suspected of Febrile Seizures

Tick-borne encephalitis (TBE) is a serious viral neuroinfection affecting humans in large areas of Europe and Asia. TBE can occur at any age, but only a few reports of TBE in infants younger than 1 year have been published. Here, we report a case of severe TBE in an 8.5-month-old boy presenting with seizures at the beginning of the neurological phase

Measurement of BBB permeability using sodium fluorescein in (A) BALB/c and (B) C57Bl/6 mice.

<p>All mice were inoculated subcutaneously with TBEV (100 pfu). BBB permeability is expressed as brain:serum ratio (%). Thirty minutes after intraperitoneal injection of sodium fluorescein, the sera and brains were processed as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0020472#s4" target="_blank">Material and Methods</a> section and the fluorescence was measured. Asterisks indicate statistically significant increases in brain:serum fluorescence in infected versus uninfected mice (p<0.05).</p

Measurement of BBB permeability using sodium fluorescein in CD8α^−/− mice.

<p>Mice were inoculated subcutaneously with TBEV (100 pfu). BBB permeability is expressed as brain:serum ratio (%). (A) Thirty minutes after intraperitoneal injection with sodium fluorescein, the sera and brains were processed as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0020472#s4" target="_blank">Material and Methods</a> section and the fluorescence was measured. Each line segment represents the mean of four samples (points). The increase in brain:serum fluorescence in infected versus uninfected mice was statistically significant (p<0.05). (B) Sodium fluorescein accumulation in the brains of CD8α^−/− before infection and at the terminal phase (i.e. phase with neurological signs) of TBE. The brains were photographed under UV illumination.</p

BBB permeability changes in the brains of TBEV-infected C57Bl/6 mice.

<p>Brains were removed from sodium fluorescein-treated mice, either uninfected (day 0) or TBEV-infected (days 10 and 11 after inoculation). The brains were photographed under UV illumination.</p

Immune/inflammatory cell accumulation and differential upregulation of cytokine/chemokine gene expression in the brain after TBEV infection.

<p>(A–C) BALB/c, (D–F) C57Bl/6, and (G–I) CD8α^−/− mice were infected subcutaneously with TBEV (100 pfu). CD8α^−/− mice were examined at the terminal stage (i.e. phase of neurological signs) of TBEV infection. Data are expressed as the mean + standard deviation of the fold increase of expression after normalization to the housekeeping gene (mouse beta actin).</p