scholarly journals Dynamic Virus-Bacterium Interactions in a Porcine Precision-Cut Lung Slice Coinfection Model: Swine Influenza Virus Paves the Way for Streptococcus suis Infection in a Two-Step Process

2015 ◽  
Vol 83 (7) ◽  
pp. 2806-2815 ◽  
Author(s):  
F. Meng ◽  
N. H. Wu ◽  
A. Nerlich ◽  
G. Herrler ◽  
P. Valentin-Weigand ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Respiratory Tract ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Content Type ◽  
Step Process ◽  
Lung Slice ◽  
Infected Cells ◽  
Ciliated Epithelial Cells

Swine influenza virus (SIV) andStreptococcus suisare common pathogens of the respiratory tract in pigs, with both being associated with pneumonia. The interactions of both pathogens and their contribution to copathogenesis are only poorly understood. In the present study, we established a porcine precision-cut lung slice (PCLS) coinfection model and analyzed the effects of a primary SIV infection on secondary infection byS. suisat different time points. We found that SIV promoted adherence, colonization, and invasion ofS. suisin a two-step process. First, in the initial stages, these effects were dependent on bacterial encapsulation, as shown by selective adherence of encapsulated, but not unencapsulated,S. suisto SIV-infected cells. Second, at a later stage of infection, SIV promotedS. suisadherence and invasion of deeper tissues by damaging ciliated epithelial cells. This effect was seen with a highly virulent SIV subtype H3N2 strain but not with a low-virulence subtype H1N1 strain, and it was independent of the bacterial capsule, since an unencapsulatedS. suismutant behaved in a way similar to that of the encapsulated wild-type strain. In conclusion, the PCLS coinfection model established here revealed novel insights into the dynamic interactions between SIV andS. suisduring infection of the respiratory tract. It showed that at least two different mechanisms contribute to the beneficial effects of SIV forS. suis, including capsule-mediated bacterial attachment to SIV-infected cells and capsule-independent effects involving virus-mediated damage of ciliated epithelial cells.

scholarly journals Capsular Sialic Acid of Streptococcus suis Serotype 2 Binds to Swine Influenza Virus and Enhances Bacterial Interactions with Virus-Infected Tracheal Epithelial Cells

2013 ◽  
Vol 81 (12) ◽  
pp. 4498-4508 ◽  
Author(s):  
Yingchao Wang ◽  
Carl A. Gagnon ◽  
Christian Savard ◽  
Nedzad Music ◽  
Mariela Srednik ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Sialic Acid ◽  
Epithelial Cells ◽  
Respiratory Tract ◽  
Bacterial Adhesion ◽  
Swine Influenza ◽  
Streptococcus Suis ◽  
Content Type ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACTStreptococcus suisserotype 2 is an important swine bacterial pathogen, and it is also an emerging zoonotic agent. It is unknown howS. suisvirulent strains, which are usually found in low quantities in pig tonsils, manage to cross the first host defense lines to initiate systemic disease. Influenza virus produces a contagious infection in pigs which is frequently complicated by bacterial coinfections, leading to significant economic impacts. In this study, the effect of a preceding swine influenza H1N1 virus (swH1N1) infection of swine tracheal epithelial cells (NTPr) on the ability ofS. suisserotype 2 to adhere to, invade, and activate these cells was evaluated. Cells preinfected with swH1N1 showed bacterial adhesion and invasion levels that were increased more than 100-fold compared to those of normal cells. Inhibition studies confirmed that the capsular sialic acid moiety is responsible for the binding to virus-infected cell surfaces. Also, preincubation ofS. suiswith swH1N1 significantly increased bacterial adhesion to/invasion of epithelial cells, suggesting thatS. suisalso uses swH1N1 as a vehicle to invade epithelial cells when the two infections occur simultaneously. Influenza virus infection may facilitate the transient passage ofS. suisat the respiratory tract to reach the bloodstream and cause bacteremia and septicemia.S. suismay also increase the local inflammation at the respiratory tract during influenza infection, as suggested by an exacerbated expression of proinflammatory mediators in coinfected cells. These results give new insight into the complex interactions between influenza virus andS. suisin a coinfection model.

scholarly journals STUDIES ON IMMUNITY TO SWINE INFLUENZA

1932 ◽  
Vol 56 (4) ◽  
pp. 575-585 ◽  
Author(s):  
Richard E. Shope
Keyword(s):  
Influenza Virus ◽  
Respiratory Tract ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Specific Relationship

Of the two etiological components of swine influenza, only the filtrable virus possessed immunizing properties. H. influenzae suis, while essential to the production of the disease, played only a secondary and contributory rôle and, alone, conferred no immunity. Serum of swine convalescent from the filtrate disease neutralized the swine influenza etiological complex of organism and virus. Intramuscularly administered swine influenza virus was incapable of inducing illness but did render hogs immune to swine influenza. It is suggested that a specific relationship, as regards infectivity, exists between the swine influenza virus and the tissues of the respiratory tract.

scholarly journals THE SWINE LUNGWORM AS A RESERVOIR AND INTERMEDIATE HOST FOR SWINE INFLUENZA VIRUS

1941 ◽  
Vol 74 (1) ◽  
pp. 49-68 ◽  
Author(s):  
Richard E. Shope
Keyword(s):  
Influenza Virus ◽  
Respiratory Tract ◽  
Intermediate Host ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Preceding Paper ◽  
Virus Infections ◽  
Single Experiment ◽  
Hog Cholera ◽  
Hog Cholera Virus

1. The swine lungworm can serve as intermediate host in transmitting swine influenza virus to swine. The virus is present in a masked non-infective form in the lungworm, however, and, to induce infection, must be rendered active by the application of a provocative stimulus to the swine it infests. Multiple intramuscular injections of H. influenzae suis furnish a means of provoking infection. Swine influenza infections can be provoked in properly prepared swine during the autumn, winter, and spring, but not during the summer. The phenomenon, while not regularly reproducible, occurs in well over half the experiments conducted outside the refractory period of summer. No explanation for the failures is apparent. 2. The virus can persist in its lungworm intermediate host for at least 2 years. 3. Swine infected with swine influenza virus by way of the lungworm intermediate host exhibit a more pronounced pneumonia of the posterior lobes of the lung than do animals infected intranasally with virus. The situation of the worms providing the virus will account for this. 4. Occasional swine infested with lungworms carrying influenza virus fail to become clinically ill after provocation but instead become immune. In these it is believed that lungworms containing the virus are localized outside the respiratory tract at the time of provocation. 5. It is believed that the experiments described furnish an explanation for the findings recorded in the preceding paper, in which swine influenza virus infections were induced in apparently normal swine by multiple injections of H. influenzae suis. 6. In a single experiment swine lungworms failed to transmit hog cholera virus.

scholarly journals Innate antiviral cytokine response to swine influenza virus by swine respiratory epithelial cells

2021 ◽  
Author(s):  
Abhijeet Bakre ◽  
Les Jones ◽  
Jackelyn Murray ◽  
Z. Beau Reneer ◽  
Victoria Meliopoulos ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Cytokine Response ◽  
Cell Type ◽  
Respiratory Epithelial Cells ◽  
Interferon Stimulated Genes ◽  
Virus Reassortment ◽  
Respiratory Epithelial

Swine influenza virus (SIV) can cause respiratory illness in swine. Swine contribute to influenza virus reassortment as avian, human, and/or SIV viruses can infect swine, reassort, and new viruses can emerge. Thus, it is important to determine the host antiviral responses that affect SIV replication. In this study, we examined the innate antiviral cytokine response to SIV by swine respiratory epithelial cells focusing on the expression of interferon (IFN) and interferon-stimulated genes (ISGs). Both primary and transformed swine nasal and tracheal respiratory epithelial cells were examined following infection with field isolates. The results show IFN and ISG expression is maximal at 12-hour post-infection (hpi) and is cell-type and virus genotype-dependent. Importance Swine are considered intermediate hosts that have facilitated influenza virus reassortment events that have given rise pandemics or genetically related viruses have become established in swine. In this study, we examine the innate antiviral response to swine influenza virus in primary and immortalized swine nasal and tracheal epithelial cells, and show virus strain and host cell-type dependent differential expression of key interferons and interferon-stimulated genes.

scholarly journals Neutrophils do not bind to or phagocytize human immune complexes formed with influenza virus

Blood ◽  
1993 ◽  
Vol 82 (5) ◽  
pp. 1639-1646 ◽  
Author(s):  
DR Ratcliffe ◽  
J Michl ◽  
EB Cramer
Keyword(s):  
Influenza Virus ◽  
Sialic Acid ◽  
Epithelial Cells ◽  
Binding Site ◽  
Immune Complexes ◽  
Human Neutrophils ◽  
Sialic Acid Binding ◽  
Infected Cells ◽  
Neutrophil Adherence ◽  
Human Immune

Abstract Neutrophils appear to form the first line of defense against influenza virus, yet it is unclear how these leukocytes recognize influenza- infected cells. While demonstrating that neutrophils adhere specifically to the sialic acid-binding site on the hemagglutinin molecule (HA) on the surface of influenza-infected (WSN[H1N1]) epithelial cells and not to other viral or epithelial cell antigens, it was observed that human neutrophils do not recognize immune complexes formed with influenza virus. Intact antibodies (mouse monoclonal antibodies [MoAbs] IgG1 and IgG2b, human immune heat-inactivated serum [predominantly IgG1], and IgG purified from human immune serum) that block the sialic acid-binding site on HA significantly reduced (> 80%) neutrophil adherence to influenza-infected epithelial cells. Binding and phagocytosis of free influenza virions and neutrophil agglutination by influenza virus were completely prevented by these antibodies. Intact and F(ab')2 fragments of mouse MoAbs to other viral epitopes caused increased neutrophil adherence to infected cells. This binding was eliminated by F(ab'2) fragments of MoAbs against the sialic acid- binding site on HA, but not by saturating amounts of MoAbs, which block the neutrophil Fc receptors. Thus, it appears that human neutrophils show little ability to bind via their Fc receptors to the immune complexes formed with antibody and either influenza-infected epithelial cells or the free virion. These findings are in contrast to the general dogma, and are the first example of antibody opsonization reducing, rather than enhancing, neutrophil binding and phagocytosis of a pathogen.

scholarly journals Epidemic Status of Swine Influenza Virus in China

2013 ◽  
Vol 54 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Weili Kong ◽  
Jiahui Ye ◽  
Shangsong Guan ◽  
Jinhua Liu ◽  
Juan Pu
Keyword(s):  
Influenza Virus ◽  
Swine Influenza Virus ◽  
Swine Influenza

scholarly journals Isolation of a Novel Swine Influenza Virus from Oklahoma in 2011 Which Is Distantly Related to Human Influenza C Viruses

2013 ◽  
Vol 9 (2) ◽  
pp. e1003176 ◽  
Author(s):  
Ben M. Hause ◽  
Mariette Ducatez ◽  
Emily A. Collin ◽  
Zhiguang Ran ◽  
Runxia Liu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Human Influenza
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