Detection of Hanta, Influenza A, and Parainfluenza Virus

Author(s):  
Ebtisam Wilkins ◽  
Ravil Sitdikov
2019 ◽  
Vol 31 (1) ◽  
pp. 44-51

Objectives of study are (1) to reinforce the national capacity for diagnosis and antibiogram of some infectious diseases causing severe acute respiratory infection (SARI) and (2) to build a network between hospital and laboratory for the diagnosis and surveillance of SARI in Yangon. This study is a crosssectional hospital- and laboratory-based descriptive study. A total of 825 samples including respiratory samples and blood samples from 511 children attending Yangon Children’s Hospital and Yankin Children’s Hospital from December 2014 to April 2016 for treatment of SARI were included. Identification and antibiotic sensitivity testing were done using Vitek 2. Out of 129 gram-negative bacilli (GNB), K. pneumoniae 32%, P. aeruginosa 18%, A. baumannii 13%, E. coli 9% were mostly isolated. Among 35 gram-positive cocci (GPC), S. aureus 42% and S. pneumoniae 6% were mostly isolated. Multidrug resistance rates were E. coli 100%, K. pneumoniae 95%, A. baumanii 82% and P. aeruginosa 17%. Extended-spectrum beta-latamase (ESBL)-producing K. pneumoniae and E. coli was 6 out of 10 tested organisms. Carbarpenemase-producing GNB and methicillin-resistant Staphylococcus aureus (MRSA) were 21% and 33%, respectively. Virology section tested 529 samples of 490 patients using the FTD33 Multiplex PCR method which can detect 33 pathogens including 20 viruses, 12 bacteria and 1 fungus. Out of 490 patients, 374 were PCR positive. Different types of samples including nasopharyngeal, throat, endotracheal and laryngeal swab, tracheal secretion and bronchoalveolar lavage, were tested. Out of 566 viruses, respiratory syncytial virus (RSV) (19.3%), rhinovirus (17.0%), parechovirus (14.3%), bocavirus (11.1%), adenovirus (10.2%), metapneumo-virus A and B (10.2%), parainfluenza virus (5.7%), enterovirus (3.0%), influenza A virus (2.8%), coronavirus (4%), parainfluenza virus (0.9%) and influenza C virus (0.4%) were detected. This study highlighted the etiological agents of bacteria, viruses and drug-resistant bacterial pathogens in SARI.


2021 ◽  
Author(s):  
Tina Meischel ◽  
Svenja Fritzlar ◽  
Fernando Villalon-Letelier ◽  
Melkamu B. Tessema ◽  
Andrew G. Brooks ◽  
...  

Interferon-induced transmembrane (IFITM) proteins inhibit a broad range of enveloped viruses by blocking entry into host cells. We used an inducible overexpression system to investigate if IFITM1, IFITM2 and IFITM3 could modulate early and/or late stages of influenza A virus (IAV) or parainfluenza virus (PIV)-3 infection in human A549 airway epithelial cells. IAV and PIV-3 represent respiratory viruses which utilise distinct cellular entry pathways. We verify entry by endocytosis for IAV, whereas PIV-3 infection was consistent with fusion at the plasma membrane. Following induction prior to infection, all three IFITM proteins restricted the percentage of IAV-infected cells at 8 hours post-infection. In contrast, prior induction of IFITM1 and IFITM2 did not inhibit PIV-3 infection, although a modest reduction was observed with IFITM3. siRNA-mediated knockdown of endogenous IFITM1, IFITM2 and IFITM3 expression, in the presence or absence of pre-treatment with type I interferon, resulted in increased IAV, but not PIV-3, infection. This suggests that while all three IFITMs display antiviral activity against IAV, they do not restrict the early stages of PIV-3 infection. IAV and PIV-3 infection culminates in viral egress through budding at the plasma membrane. Inducible expression of IFITM1, IFITM2 or IFITM3 immediately after infection did not impact titres of infectious virus released from IAV or PIV-3 infected cells. Our findings show that IFITM proteins differentially restrict the early stages of infection of two respiratory viruses with distinct cellular entry pathways, but do not influence the late stages of replication for either virus. IMPORTANCE Interferon-induced transmembrane (IFITM) proteins restrict the initial stages of infection for several respiratory viruses, however their potential to modulate the later stages of virus replication has not been explored. In this study we highlight the utility of an inducible overexpression system to assess the impact of IFITM proteins on either early or late stage replication of two respiratory viruses. We demonstrate antiviral activity by IFITM1, IFITM2 and IFITM3 against influenza A virus (IAV) but not parainfluenza virus (PIV)-3 during the early stages of cellular infection. Furthermore, IFITM induction following IAV or PIV-3 infection does not restrict the late stages of replication of either virus. Our findings show that IFITM proteins can differentially restrict the early stages of infection of two viruses with distinct cellular entry pathways, yet do not influence the late stages of replication for either virus.


2005 ◽  
Vol 79 (11) ◽  
pp. 6674-6679 ◽  
Author(s):  
Yasuko Maeda ◽  
Masato Hatta ◽  
Ayato Takada ◽  
Tokiko Watanabe ◽  
Hideo Goto ◽  
...  

ABSTRACT Influenza and human parainfluenza virus infections are of both medical and economical importance. Currently, inactivated vaccines provide suboptimal protection against influenza, and vaccines for human parainfluenza virus infection are not available, underscoring the need for new vaccines against these respiratory diseases. Furthermore, to reduce the burden of vaccination, the development of multivalent vaccines is highly desirable. Thus, to devise a single vaccine that would elicit immune responses against both influenza and parainfluenza viruses, we used reverse genetics to generate an influenza A virus that possesses the coding region for the hemagglutinin/neuraminidase ectodomain of parainfluenza virus instead of the influenza virus neuraminidase. The recombinant virus grew efficiently in eggs but was attenuated in mice. When intranasally immunized with the recombinant vaccine, all mice developed antibodies against both influenza and parainfluenza viruses and survived an otherwise lethal challenge with either of these viruses. This live bivalent vaccine has obvious advantages over combination vaccines, and its method of generation could, in principle, be applied in the development of a “cocktail” vaccine with efficacy against several different infectious diseases.


2020 ◽  
Vol 29 (3) ◽  
pp. 129-136
Author(s):  
Safaa M. EL-Ageery ◽  
Rabab A. Ali ◽  
Mayada S. Zeid

Background: In children with primary immunodeficiency (PID), the most common types of infection are respiratory tract infections, among which viral pneumonia representing the majority. Early diagnosis and treatment can prevent or diminish the respiratory complications. Multiplex polymerase chain reaction (Multiplex PCR) can permit amplification of a lot of viruses all together in a single reaction mixture. Objective: Determining different viruses causing pneumonia in children with PID by multiplex PCR. Methodology: A cross-sectional study included 33 nasopharyngeal swabs collected from children suffering from PID with clinical respiratory signs of pneumonia. For each collected sample, nucleic acid extraction and multiplex PCR were done using primers specific for influenza A, influenza B, adenovirus, respiratory syncytial virus (RSV), cytomegalovirus (CMV), parainfluenza virus 1 (PIV1), parainfluenza virus 2 (PIV2), parainfluenza virus 3 (PIV3) and human coronavirus (HCoV-NL63). Results: Viruses were detected in 11 nasopharyngeal samples (11/33, 33.33%). Viral pneumonia was mostly found in children with severe combined immune deficiency (5/11; 45.45%), followed by children with common variable immunodeficiency (3/11; 27.27%) and children with hyper Ig E syndrome, hyper Ig M syndrome and selective Ig A deficiency (1/11; 9.09%) for each. RSV and CMV were the most common detected viruses; each virus was detected in 3 cases. Influenza virus A was detected in 2 cases and adenovirus, PIV1 and PIV3 each was detected in one case. Influenza virus B, PIV2 and HCoV-NL63 were not detected in any sample. No viruses were detected in the nasopharyngeal swabs taken from children with chronic granulomatous disease. No mixed viral infection was detected in any sample. Conclusion: Severe viral pneumonia is frequent in the children with PID. Multiplex PCR has a major benefit, as it allows simultaneous amplification of several viruses in a single reaction mixture with cost-effective diagnosis.


2014 ◽  
Vol 89 (3) ◽  
pp. 1537-1549 ◽  
Author(s):  
Kari L. Roberts ◽  
Balaji Manicassamy ◽  
Robert A. Lamb

ABSTRACTIn the extracellular environment, cell-free virions seek out naive host cells over long distances and between organisms. This is the primary mechanism of spread for most viruses. Here we provide evidence for an alternative pathway previously undescribed for orthomyxoviruses, whereby the spread of influenza A virus (IAV) infectious cores to neighboring cells can occur within intercellular connections. The formation of these connections requires actin dynamics and is enhanced by viral infection. Connected cells have contiguous membranes, and the core infectious viral machinery (RNP and polymerase) was present inside the intercellular connections. A live-cell movie of green fluorescent protein (GFP)-tagged NS1 of IAV shows viral protein moving from one cell to another through an intercellular connection. The movement of tagged protein was saltatory but overall traveled only in one direction. Infectious virus cores can move from one cell to another without budding and release of cell-free virions, as evidenced by the finding that whereas a neuraminidase inhibitor alone did not inhibit the development of IAV microplaques, the presence of a neuraminidase inhibitor together with drugs inhibiting actin dynamics or the microtubule stabilizer paclitaxel (originally named taxol) precluded microplaque formation. Similar results were also observed with parainfluenza virus 5 (PIV5), a paramyxovirus, when neutralizing antibody was used to block spread by cell-free virions. Intercellular spread of infectious core particles was unaffected or enhanced in the presence of nocodazole for IAV but inhibited for PIV5. The intercellular connections have a core of filamentous actin, which hints toward transport of virus particles through the use of a myosin motor.IMPORTANCEHere we describe a new method by which influenza A virus (IAV) spreads from cell to cell: IAV uses intracellular connections. The formation of these connections requires actin dynamics and is enhanced by viral infection and the absence of microtubules. Connected cells appeared to have contiguous membranes, and the core infectious viral machinery (RNP and polymerase) was present inside the intercellular connections. Infectious virus cores can move from one cell to another without budding and release of cell-free virions. Similar results were also observed with parainfluenza virus 5 (PIV5).


2013 ◽  
Vol 87 (17) ◽  
pp. 9604-9609 ◽  
Author(s):  
Z. Li ◽  
J. D. Gabbard ◽  
A. Mooney ◽  
Z. Chen ◽  
S. M. Tompkins ◽  
...  

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