scholarly journals Role of the Low-Density Lipoprotein Receptor in Entry of Bovine Viral Diarrhea Virus

2006 ◽  
Vol 80 (21) ◽  
pp. 10862-10867 ◽  
Author(s):  
Thomas Krey ◽  
Etienne Moussay ◽  
Heinz-Jürgen Thiel ◽  
Till Rümenapf

ABSTRACT Among several proposed cellular receptors for bovine viral diarrhea virus (BVDV), the low-density lipoprotein (LDL) receptor is of special interest because it is also considered a receptor for the related hepatitis C virus. It has been reported that an anti-LDL receptor monoclonal antibody blocked the infection of bovine cells by BVDV and that the resistance of bovine CRIB cells (cells resistant to infection with BVDV) (E. F. Flores and R. O. Donis, Virology 208:565-575, 1995) to BVDV infection was due to a lack of the LDL receptor (V. Agnello et al., Proc. Natl. Acad. Sci. USA 96:12766-12771, 1999). In connection with our studies on BVDV entry, we reevaluated the putative role of the LDL receptor as a cellular receptor for BVDV. It was first clearly demonstrated that neither of two monoclonal antibodies against the LDL receptor inhibited BVDV infection of two bovine cell lines. Furthermore, the LDL receptor was detected on the surface of CRIB cells. The functionality of the LDL receptor on CRIB cells was demonstrated by the internalization of fluorescently labeled LDL. In conclusion, at present no experimental evidence supports an involvement of the LDL receptor in BVDV invasion.

2015 ◽  
Vol 16 (1) ◽  
pp. 4-14 ◽  
Author(s):  
Christopher C. L. Chase ◽  
Neelu Thakur ◽  
Mahmoud F. Darweesh ◽  
Susan E. Morarie-Kane ◽  
Mrigendra K. Rajput

AbstractBovine viral diarrhea virus (BVDV) has long been associated with a wide variety of clinical syndromes and immune dysregulation, many which result in secondary bacterial infections. Current understanding of immune cell interactions that result in activation and tolerance are explored in light of BVDV infection including: depletion of lymphocytes, effects on neutrophils, natural killer cells, and the role of receptors and cytokines. In addition, we review some new information on the effect of BVDV on immune development in the fetal liver, the role of resident macrophages, and greater implications for persistent infection.


2011 ◽  
Vol 24 (1) ◽  
pp. 51-64 ◽  
Author(s):  
Ingeborg M. Langohr ◽  
Gregory W. Stevenson ◽  
Eric A. Nelson ◽  
Stephen D. Lenz ◽  
Huiling Wei ◽  
...  

The role of Bovine viral diarrhea virus (BVDV) in the development of Porcine circovirus-2 (PCV-2)-associated disease (PCVAD) was investigated in 2 experimental studies. In the first, separate groups of germ-free pigs were inoculated with filtered tissue homogenate (from diseased pigs) containing PCV-2b + BVDV-1–like virus (group 1), PCV-2a + BVDV-1–like virus (group 4), BVDV-1–like virus only (group 3), or PCV-2b + BVDV-1–like virus following a BVDV vaccination protocol (group 2). This last group was used to test if BVDV vaccination would prevent clinical PCVAD in this model. Many of the inoculated pigs had mild multisystemic inflammation consistent with classic PCVAD. One vaccinated, dually inoculated pig had acute respiratory distress followed by death at 21 days postinfection. Lesions in this pig resembled the severe form of PCVAD observed in the field since the fall of 2004, suggesting a role of ruminant pestiviruses and/or vaccination in the development of this disease. In the second study, cesarean-derived, colostrum-deprived pigs were inoculated with PCV-2b and a cytopathic strain of BVDV-1 (cpBVDV-NADL) either alone or in combination. Clinical signs of PCVAD were seen in a single animal inoculated only with PCV-2b. This pig had growth retardation followed by acute respiratory distress leading to death 30 days postinfection. Pulmonary lesions in this animal were similar to those seen in the pig that died in the first study. Infection with cpBVDV-NADL did not enhance PCV-2b replication or lesion formation.


2002 ◽  
Vol 63 (10) ◽  
pp. 1455-1463 ◽  
Author(s):  
Martha J. Harding ◽  
Xuemei Cao ◽  
Homayoun Shams ◽  
Anthony F. Johnson ◽  
Ventzislav B. Vassilev ◽  
...  

2009 ◽  
Vol 90 (11) ◽  
pp. 2650-2659 ◽  
Author(s):  
Miriam Pedrera ◽  
José C. Gómez-Villamandos ◽  
José L. Romero-Trevejo ◽  
María A. Risalde ◽  
Verónica Molina ◽  
...  

The mechanisms responsible for lymphocyte apoptosis in bovine viral diarrhoea have not yet been clarified. Previous work suggests that bovine viral diarrhea virus (BVDV) is only directly responsible for the destruction of a small number of lymphocytes. The aim of this study was to clarify, in vivo, the role of macrophages in lymphocyte destruction through indirect mechanisms linked to the biosynthetic activation of these immunocompetent cells on ileal Peyer's patches, as well as the distribution and quantification of apoptosis. Eight colostrum-deprived calves were inoculated intranasally with a non-cytopathic strain of BVDV genotype 1 and killed in batches of two at 3, 6, 9 and 14 days post-inoculation (p.i.). The progressive depletion of Peyer's patches was found to be due to massive lymphocyte apoptosis, with an increase in cleaved caspase-3 and TUNEL-positive cells. Lymphoid depletion was accompanied, from 3 days p.i., by a significant rise in macrophage numbers both in lymphoid follicles and in interfollicular areas. Some macrophages showed signs of viral infection, together with subcellular changes indicative of phagocyte activation and, in some cases, of secretory activity. However, the number of macrophages that showed positive immunostaining for tumour necrosis factor-α and interleukin-1α, cytokines with a proven ability to induce apoptosis, remained low throughout the experiment in lymphoid follicles, where most apoptotic cells were found. These results thus appear to rule out a major involvement of macrophages and macrophage-secreted chemical mediators in the apoptosis of follicular B lymphocytes during BVDV infection.


Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 600 ◽  
Author(s):  
Luís Guilherme de Oliveira ◽  
Marina L. Mechler-Dreibi ◽  
Henrique M. S. Almeida ◽  
Igor R. H. Gatto

Bovine viral diarrhea virus (BVDV) is an important pathogen belonging to the Pestivirus genus, Flaviviridae family, which comprises viral species that causes an economic impact in animal production. Cattle are the natural host of BVDV and the main source of infection for pigs and other animal species. Due to its antigenic and genetic similarity with other important pestiviruses such as Classical Swine Fever Virus (CSFV), several studies have been conducted to elucidate the real role of this virus in piglets, sows, and boars, not only in the field but also in experimental infections, which will be discussed in this paper. Although BVDV does not pose a threat to pigs as it does to ruminants, the occurrence of clinical signs is variable and may depend on several factors. Therefore, this study presents a survey of data on BVDV infection in pigs, comparing information on prevalence in different countries and the results of experimental infections to understand this type of infection in pigs better.


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