Disease relevance of Paramyxoviridae Infections

• We show that mice lacking the chemokine Ccl5 are immune compromised to the point of delayed viral clearance, excessive airway inflammation and respiratory death after mouse parainfluenza or human influenza virus infection [1].
• In contrast, human parainfluenza type 3 or herpes simplex virus type 1 infections did not increase arachidonate metabolism [2].
• In the present study, using bacterially expressed unphosphorylated P protein of Sendai virus, a mouse parainfluenza virus, we have shown that the major cellular kinase that phosphorylates P protein in vitro is biochemically and immunologically indistinguishable from protein kinase C (PKC) zeta isoform [3].
• There were eight cases of adenovirus type 5, two cases of respiratory syncytial virus (RSV), and one case of parainfluenza virus type 2 [4].
• The fusion glycoprotein (F) and hemagglutinin-neuraminidase (HN) genes of human parainfluenza virus type 2 (PI2) were molecularly cloned and expressed in HeLa-T4 cells by using the vaccinia virus-T7 transient expression system [5].

High impact information on Paramyxoviridae Infections

• Persistent parainfluenza virus shedding during isolation at the South Pole [6].
• Cellular protein kinase C isoform zeta regulates human parainfluenza virus type 3 replication [7].
• Crystals of hemagglutinin-neuraminidase of parainfluenza virus contain triple-stranded helices [8].
• In contrast the SV5 F glycoprotein and the HN glycoprotein of the highly related parainfluenza virus 3 (hPIV-3) were found only on the cell surface [9].
• Specific interaction in vitro and in vivo of glyceraldehyde-3-phosphate dehydrogenase and LA protein with cis-acting RNAs of human parainfluenza virus type 3 [10].

Chemical compound and disease context of Paramyxoviridae Infections

• Relative affinity of the human parainfluenza virus type 3 hemagglutinin-neuraminidase for sialic acid correlates with virus-induced fusion activity [11].
• 4-GU-DANA (zanamivir) (as well as DANA and 4-AM-DANA) was found to inhibit the neuraminidase activity of human parainfluenza virus type 3 (HPF3) [12].
• The intracellular synthesis of human parainfluenza type 3 virus-specified polypeptides was examined by polyacrylamide gel electrophoresis of [35S]methionine-labeled cell extracts under reducing conditions [13].
• Human parainfluenza virus type 3 HN-receptor interaction: effect of 4-guanidino-Neu5Ac2en on a neuraminidase-deficient variant [14].
• Role of NH(2)- and COOH-terminal domains of the P protein of human parainfluenza virus type 3 in transcription and replication [15].

Biological context of Paramyxoviridae Infections

• We cloned and determined the nucleotide sequences of cDNAs against genomic RNA encoding the L protein of human parainfluenza type 2 virus (PIV-2) [16].
• Nucleotide sequence of the bovine parainfluenza 3 virus genome: the genes of the F and HN glycoproteins [17].
• Antibody responses of humans and nonhuman primates to individual antigenic sites of the hemagglutinin-neuraminidase and fusion glycoproteins after primary infection or reinfection with parainfluenza type 3 virus [18].
• The nucleotide sequence of mRNA for the hemagglutinin-neuraminidase (HN) protein of human parainfluenza type 3 virus obtained from the corresponding cDNA clone had a single long open reading frame encoding a putative protein of 64,254 daltons consisting of 572 amino acids [19].
• Membrane fusion promoted by increasing surface densities of the paramyxovirus F and HN proteins: comparison of fusion reactions mediated by simian virus 5 F, human parainfluenza virus type 3 F, and influenza virus HA [20].

Anatomical context of Paramyxoviridae Infections

• Intercellular adhesion molecule-1 (ICAM-1)-dependent and ICAM-1-independent adhesive interactions between polymorphonuclear leukocytes and human airway epithelial cells infected with parainfluenza virus type 2 [21].
• Human epithelial cells infected with the parainfluenza virus simian virus 5 (SV5) show minimal activation of host cell interferon (IFN), cytokine, and cell death pathways [22].
• These findings indicated that the syncytium formation by bovine parainfluenza 3 virus requires both the F and HN proteins and that the extensive syncytium formation by the M virus is due to the M virus HN protein [23].
• A cell-free system supporting transcription, replication, and nucleocapsid assembly of the genome RNA of human parainfluenza virus type 3 (HPF3) is described [24].
• CONCLUSION: Infections with RSV as well as with influenza and parainfluenza virus during early infancy preferentially promote a TH2-like response in the nose with local production of IL-4, IL-5, and macrophage inflammatory protein 1beta and infiltration and activation of eosinophils [25].

Gene context of Paramyxoviridae Infections

• Human parainfluenza type 2 virus (hPIV-2)-infected HeLa (HeLa-CA) cells and hPIV-2 V-expressing HeLa (HeLa-V) cells show high resistance to alpha/beta interferons (IFN-alpha/beta) irrespective of whether vesicular stomatitis virus or Sindbis virus is used as a challenge virus [26].
• Human parainfluenza virus type 3 up-regulates major histocompatibility complex class I and II expression on respiratory epithelial cells: involvement of a STAT1- and CIITA-independent pathway [27].
• We demonstrate that cellular expression of V proteins from simian virus 5 (SV5) and type II human parainfluenza virus (HPIV2) induces polyubiquitylation of STAT1 and STAT2 targets [28].
• Infection of cells with type 2, but not type 1 or type 3 human parainfluenza virus (HPIV) leads to a loss of cellular STAT2 protein [29].
• Although these proteins are considered accessory, numerous studies have highlighted the importance of these proteins in virus transcription and interferon signaling, including our previous observation on the role of human parainfluenza virus type 3 (HPIV 3) C protein in the transcription of viral genome (Malur et al., Virus Res. 99:199-204, 2004) [30].

Analytical, diagnostic and therapeutic context of Paramyxoviridae Infections

• A parainfluenza type 1 virus (6/94) recovered from brain cell cultures of two patients with multiple sclerosis (MS) was inoculated into newborn chimpanzees by the intranasal (IN) or intracerebral (IC) routes [31].
• Crystallization of biologically active hemagglutinin-neuraminidase glycoprotein dimers proteolytically cleaved from human parainfluenza virus type 1 [32].
• The CSF from 279 patients with multiple sclerosis (MS), probable MS, or controls was examined by radioimmunoassay (RIA) for antibodies to measles, rubella, mumps, parainfluenza 1 (Sendai) (strain 6/94), herpes simplex (HSV), varicella, and vaccinia viruses [33].
• Human parainfluenza type 3 (PI3) virus was incorporated into microspheres composed of a biocompatible and biodegradable DL-lactide and glycolide copolymer [34].
• Molecular cloning and sequence analysis of the fusion glycoprotein gene of human parainfluenza virus type 2 [35].

References