Veterinary Research

Veterinary Research

Persons using assistive technology might not be able to fully access information in this file. Cornelius? Please get a full exam with MD. Problem/Condition: Acquired immunodeficiency syndrome (AIDS)-defining opportunistic illnesses (OIs) are the major cause of morbidity and mortality among persons infected with human immunodeficiency virus (HIV). The laboratory also develops novel vaccines and therapeutics based upon the Herpes simplex virus (HSV) amplicon vector platform for future clinical implementation. Among the most common known supplements to resist infections or viruses is Inositol. Encephalitis was a significant diagnosis in 9% (7/74) of porpoises in this study, 3% (4/133) of porpoises stranded along the German coast [17], and 11% (6/55) of porpoises stranded along the Belgian coast [15].

Literature from the United States in the 1960s suggested that PVE occurs 9–59 times for every 1 million vaccinations [3]. I am interested in women, and looking for a “friend” someone who is cool, positive. With the patient reporting increasing odynophagia (pain on swallowing) and the chest pain occurring most frequently after eating, a gastroscopy was performed, showing a massive ulcerous esophagitis with sprinkled whitish plaques. Cancer virotherapy is an old concept that arose from observations of unexpected tumor regressions coinciding with virus infections. In order to establish a primary infection and be maintained in the host population, the alphaherpesviruses must be able to evade both innate and acquired immune defenses with some efficiency. These indirect OV-induced oncolytic effects can result from tumor vasculature disruption and angiogenesis, release of toxic cytokines from infected tumor-resident or infiltrating immune cells, and even more importantly, from systemic anti-tumor immune responses. Infections with autonomous parvoviruses, to which the well-studied minute virus of mice (MVM) and the closely related H-1 virus belong, is strictly dependent on host cell functions expressed during the S-phase of the cell cycle but does not require helper virus factors (18,62, 68).

Additionally, some are encoded by virus genes. Nascent virions are released from the cell surface by the action of the viral neuraminidase (NA) glycoprotein (18, 20, 21). For other picornaviruses, such as foot-and-mouth disease virus (FMDV) and some echoviruses, there is evidence for participation of additional cell surface molecules in virus entry, heparan sulfate and β2-microglobulin, respectively (7). Active PKR phosphorylates the alpha subunit of initiation factor 2 (eIF2α), leading to inhibition of translation initiation and thus aborting virus multiplication. PPHV-2, the striped dolphin herpesvirus and the bottlenose dolphin herpesvirus belong to the subfamily of Alphaherpesvirinae, suggesting that these viruses have a tropism for the nervous system and are potentially pathogenic in cetaceans. Both trials met their primary endpoint of improved overall survival in patients receiving nivolumab compared to chemotherapy. The next herpesvirus we detected in these harbor porpoises, PPHV-1, was associated with a plaque in the clitoral mucosa of an adult female harbor porpoise (animal #6; Table 1).
Veterinary Research

The cytopathic effect caused by H-1 virus, as well as viral macromolecular synthesis and virus production, were analyzed. In vivo, selective neuronal expression of hsp70 enhances the IFN-β response to intracranial MeV inoculation, reducing mortality in H-2d congenic C57BL/6 mice (11). In contrast to these genital plaques, van Beurden et al. Another therapeutic approach aimed to achieve an improved outcome by combining sequential intratumoral injections of oncolytic HSV-1 and immature dendritic cells. Genital lesions associated with herpesvirus infection have been found in four other cetacean species: a male Blainville’s beaked whale (Mesoplodon densirostris) [29], a female Risso’s dolphin (Grampus griseus) [9], a male striped dolphin [30] and both male and female bottlenose dolphins [9, 31, 32]. In the Blainville’s beaked whale [29], the bottlenose dolphin [32] and the striped dolphin [30], the mucosal lesions were histologically similar to those reported in harbor porpoise #6: a well-demarcated area of epithelial hyperplasia, characterized by INIB in affected epithelial cells. A number of avirulence genes have been cloned from Xcv (Minsavage et al., 1990), one of which is avrBs3.

In a zoo collection of bottlenose dolphins, infection was endemic and seroconversion occurred around the age of onset of sexual behavior [32]. This epidemiological observation, together with the predilection for the genital mucosa, indicates that sexual contact is an important route of transmission of gammaherpesviruses in cetaceans. There is ongoing debate about the roles of herpesvirus infection and papillomavirus infection as the cause of genital lesions in cetaceans [33]. In that perspective, it is of interest that papillomavirus was detected in a skeletal muscle sample of harbor porpoise #6 by next-generation sequencing. Although we did not detect papillomavirus by PCR in the clitoral plaque sample of this animal, it cannot be excluded that the primers used—based on papillomaviruses from Burmeister’s porpoise—are not suited to detection of papillomavirus of harbor porpoises. Dolori intensi ed arrossamenti accompagnano pure il glaucoma, patologia causata da aumento della pressione all’interno dell’occhio. Il processo si può estendere dalla membrana di Bowmann a quella di Descemet (strati della cornea).

Despite detection in brain, pulmonary lymph node, genital slit and blowhole samples of several porpoises (animals #1, #3, #4, #5, #7 and #8; Table 1), no association with pathologic changes in the respective tissues was observed. It remains to be determined why PPHV-3 had an apparent predilection for juvenile male harbor porpoises and what the pathogenic potential of this virus is. Because this research was part of a long-term study of morbidity and mortality factors in live-stranded harbor porpoises, we had a substantial sample size to evaluate the prevalence of both herpesvirus-associated encephalitis and genital plaques. The prevalence of PPHV-2-associated encephalitis was low (1%; 1/74), indicating that this morbidity factor is rare in harbor porpoises that strand alive on the Dutch and adjacent coasts. However, a caveat is that only one brain sample (a sample of cerebral tissue and a sample of cerebellar tissue in one vial) was collected for virological analysis as part of our standard autopsy protocol. Given that herpesvirus infections may be limited to certain areas of the brain [34], we may have underestimated the number of porpoises with PPHV-2 in the brain. The low prevalence of herpesvirus-associated genital plaques in live-stranded harbor porpoises—0% (0/52) in juvenile and adult males, 2% (1/46) in juvenile and adult females—contrasts with the much higher prevalence in bottlenose dolphins in a zoo collection—23% (3/13) in juvenile and adult males, 27% (4/15) in juvenile and adult females [32].

L’uso della fluoresceina aiuta a definire i margini dell’ulcera corneale e può rivelare dettagli aggiuntivi dell’epitelio circostante. Possible explanations are differences in herpesvirus, host species, or captive versus free-living populations. Detailed information about all assessments, study recruitment, access and ethical issues, including support for participants testing HIV positive, is published elsewhere [21]. For example, herpes simplex virus 1 in human beings establishes a latent infection in the root ganglia of the trigeminal nerve [35]. When a tumor met both these criteria, the mouse entered the experiment and was randomly designated to one of the three treatment groups (AdMLP.Apoptin, AdCMV.LacZ, or virus dilution buffer). Such a serological assay, based on cultured virus, was successfully developed to detect specific antibodies against Tursiops truncatus herpesvirus in bottlenose dolphin sera [32].

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Veterinary Research

Veterinary Research

To investigate the impact of pregnancy on human herpesvirus 8 (HHV-8) reactivation in human immunodeficiency virus type 1 (HIV-1)-infected women, the HHV-8 DNA presence and load were analyzed in peripheral blood mononuclear cells (PBMCs) and cervicovaginal secretions (CVSs) from 15 pregnant women coinfected with HIV-1 and HHV-8. Induction of PERV antigen in porcine peripheral blood mononuclear cells by human herpesvirus 1. Subsequent elongation of this short poly(A) tail requires poly(A)-binding protein II, CPSF complex and PAP (PABII), which facilitate rapid, processive poly(A) addition. A. This protein was identified as gH by selective depletion with an anti-gH monoclonal antibody, as well as by immunoblot analysis with a rabbit hyperimmune serum directed against a gH synthetic peptide. Moreover, if the genomes are intact, there could be gene expression from over 85 viral genes in each cell as well as the potential for reactivated infectious virus [6,7]. Arguments for a viral etiology have been presented for these diseases.19,20 Our objectives were two-fold: first, to quantify virus loads of known HHVs capable of infecting lymphocytes (EBV, HHV-8, HHV-6 variants A and B, HHV-7) and also CMV using qPCR; second to search for the presence of new herpesviruses using CODEHOP PCR.

Similarly, all but one of the beta and gamma CHPKs displayed bona fide Cdk activity in S. Immunohistochemistry was more sensitive than the histological demonstration of cytomegalovirus or measles virus inclusions. Use of a suboptimal insertion site can have a pronounced effect on vaccine efficacy. Another component of the fusion mechanism is gK, which also interacts with gB by binding to its amino terminus and modifying the ability of this glycoprotein to mediate “viral-envelope-to-cellular-membrane fusion” [32]. Human herpesvirus 1 encephalitis should be considered as a differential diagnosis for rabbits with neurologic disease. Glycoprotein D of both BoHV-1 and BoHV-5 consists of approximately 417 aa, with 79.9% amino acid (aa) identity [34], N- and O-linked oligosaccharides, and a molecular weight of approximately 71 kDa [35]. It is a type I membrane glycoprotein, with a signal sequence and a cleavage site located between aa 18 and 19 in BoHV-1 gD and between aa 19 and 20 in BoHV-5 gD, based on the position, length, relative hydrophobicity and consensus cleavage site characteristic of a signal sequence [36].

This signal sequence is cleaved to yield a mature protein of 399 aa. The amino-terminal portion of gD comprises the extracellular domain, while its carboxy-terminus consists of a hydrophobic transmembrane anchor sequence and a cytoplasmic tail of approximately 28 aa in BoHV-1 gD and 35 aa in BoHV-5 gD [35],[37]. The nucleotide sequence of this glycoprotein gene has a GC nucleotide content of 70% [ 35 ], similar to Suid herpesvirus 1 (SuHV-1) (75%) and HHV-1 (65%) gD homologues [ 38 ]. Initial studies on vertical transmission showed that HHV-8 seroreactivity in newborns is mainly due to transplacental passage of maternal antibodies (6, 18). Alignment of both gDs showed that the amino-terminal two-thirds (aa 1-282) of BoHV-1 [ 35 ],[ 39 ] and BoHV-5 [ 36 ] gD are relatively well conserved (Figure 1 ). However, the difference between gD from these viruses maps to a glycine-rich stretch located in the molecule’s C-terminal part of the ectodomain (aa 280 and 330), in close vicinity to the transmembrane region [ 34 ],[ 36 ]. This region is characterized by a major hydrophilic peak in the case of BoHV-1 gD and may be important for interactions of the protein with other molecules of the virus, host cell or both through ionic interactions [ 37 ].

CD46 is a member of the regulators of complement activation (RCA) protein family. This shows CiHHV-6A/B effects may originate from infancy, and could result in chronic states in the adult, therefore it is important to understand the origins, distinctions and interactions with infectious virus of these integrated, inherited genomes. BoHV-1 gD [GenBank:CAA80604.1] [39] and BoHV-5 gD [GenBank:AAA67359.1] [36] were aligned with Clustal Omega v. In fact, kinases are now targets for lung and breast cancer chemotherapies [2], and importantly, for herpesviral infections as well [3], [4]. Thus, in many cases, no viral agent can be demonstrated. For global genome mutagenesis studies, transposition has previously been proven to be a valuable tool, since the random insertion of transposon sequences allows for the efficient generation of a library of unique insertional mutants. Solid and dashed lines show presumed signal sequences and transmembrane anchor sequences, respectively.

An arrow indicates the position of the BoHV-1-gD signal peptide cleavage site (aa 18 and 19) [35]. Four antigenic domains have been described for BoHV-1 gD [41], and five epitopes, three interrelated and two independent, have been reported as targets of neutralizing antibodies [42]. Monoclonal antibodies developed to epitopes located between amino acids 52-116 (MAb 3402) and 165-216 (MAb R54) do not recognize BoHV-5 gD, suggesting that these epitopes are located in the corresponding altered amino acids in BoHV-5 gD [36]. The most well characterized homologue is HHV-1 gD, the ectodomain of which is formed by a core with a variable-type immunoglobulin fold (IgV) wrapped by a N-terminal extension and a C-terminal proline-rich extension [43]. With respect to its glycosylation, differences are observed in the N-linked oligosaccharide (N-CHO) distribution for gD. HHV-1 and BoHV-1 gD possess three N-CHO sites (amino acids position 41, 102 and 411 of BoHV-1 gD), while BoHV-5 gD has only two potential sites in its sequence, one being located in its cytoplasmic tail (amino acids 102 and 411 of BoHV-5 gD) [36]. Blood and CVS specimens were processed as described previously (5).
Veterinary Research

Enzymatic deglycosylation of gD from BoHV-1 suggests that the addition of carbohydrates could mask epitopes involved in T cell recognition. This was observed after injection of native or deglycosylated forms of gD in rabbits and measurement of the delayed-type hypersensitivity (DTH) response where a stronger DTH reaction in deglycosylated gD-vaccinated rabbits was observed. In contrast, the total antibody response to gD after carbohydrate removal was lower than the response observed for native gD-vaccinated animals; however, the neutralizing antibody response and the ability of the antibodies to mediate cell lysis were not significantly reduced, indicating that most functional epitopes on this glycoprotein are carbohydrate-independent [44]. NIH 3T3 cells were maintained in Dulbecco’s modified Eagle’s medium supplemented with 10% fetal bovine serum, 2 mm l-glutamine, and 10 μg/ml gentamicin). Long range PCR was used to generate overlapping amplicons, 1–7 kb in length, across the entire CiHHV-6A genomes using primers based on reference HHV-6A strains U1102, GS, and AJ genome sequences as described [23]. However, cells expressing heparin sulfate-modified 3-O-sulfotransferases or the HVEM receptor are not susceptible to BoHV-1 (reviewed in 2000 by Spear et al. Sixteen of these are grouped into three distinct families, (Us3, UL13 and thymidine kinase) based on amino acid sequence homology ().

After diagnosis by surgical lung biopsy, all the patients received corticosteroid. Recovery of virus from transposed clones was assessed by observing characteristic MeHV-1 cytopathic effect (CPE) using light microscopy, and whenever possible, by detecting the expression of enhanced green fluorescent protein (eGFP) using fluorescent microscopy (the MuA transposon used to generate MuAΔ48-84 contained an eGFP transgene) (Fig. The gD-binding region of nectin-1 is localized at the V-like domain [50]. Studies performed with soluble forms of gD from HHV-1, HHV-2 and SuHV-1 showed efficient binding to truncated forms of nectin-1 retaining only the V-like domain; this binding was blocked by monoclonal antibodies specific for epitopes located in this domain [51],[52]. However, a study performed with chimeras that combine the V-like domain of nectin-1α with C-like domains from nectin-2α demonstrates that the V-like domain is required for full entry activity of BoHV-1, HHV-1 and -2, and SuHV-1, only when this domain is linked to two C-domains [53]. Despite the ability of gD to bind to the V-like domain, attachment does not result in viral entry, suggesting that binding of gD induces conformational changes in both gD and the receptor. This study also suggests that, based on competitive interactions, the regions on nectin-1 to which gD from different alphaherpesviruses binds, are overlapping but not necessarily identical [53].

The function of nectins as adhesion molecules that are mostly located at cell junctions suggests a key role in cell-to-cell spread of alphaherpesviruses to neurons of the peripheral and central nervous systems, as well as in the epithelium [45],[54]. Binding of gD to nectin-1 during later phases of HHV infection correlates with down-regulation of nectin-1 in cells susceptible to HHV endocytosis. All results are reported as the log10 number of HIV-1 RNA copies per milliliter of plasma or CVS. The cell-bound gD or gD from egressing virions could then mediate internalization of nectin-1 directing HHV to an endocytic pathway during entry [45]. Madin Darby bovine kidney (MDBK) cells expressing gD from BoHV-1 resist infection by heterologous virus, such as HHV-1 or SuHV-1, a phenomenon termed interference, which occurs at the level of penetration into cells [55]. However, these cells are still susceptible to BoHV-5, demonstrating an absence of interference, even though the presence of gD inhibited increase in plaque size. Immunological Reagents—Immunoprecipitation reactions were performed with monoclonal antibodies (mAbs).

For reference mapping contigs were ordered using references genomes from HHV-6A strains U1102, GS (KC465951.1) and AJ, together with manual adjustments using Artemis [37,38]. Also, a cell type known as J1.1-2 cells, which does not express any form of nectin and is resistant to HHV and BoHV-1 infection, is susceptible to BoHV-5 infection, reinforcing the idea that BoHV-5 gD can interact with a different range of receptors than those used by BoHV-1 [34]. Importantly, all the beta- and gamma-herpesvirus CHPKs, with the exception of the HHV-8 (KSHV) ORF36 protein, displayed authentic Cdk function in the yeast complementation assay. Positive expression of EBV, CMV, ADV, HCV, RSV, HHV-1, HHV-2, and MV were indicated by brown cytoplasmic or nuclear staining. The LORF5 gene was found to be non-essential for viral replication in cell culture, since CPE was observed for the disruption mutants pMeHV1-C18-MuAΔ59 and MuAΔ82. The immunology of BoHV-1 infection was reviewed in 1996 [21], and very few studies have been performed to elucidate the immune response induced by BoHV-5 infection. However, due to the similarities between both viruses, it is reasonable to expect that most of what was discovered for BoHV-1 may apply to BoHV-5 (reviewed in [8]).

The first step in an immune response to a virus infection is to avoid the interaction between virus and permissive cells; however, during primary infection, antibodies are not available to interfere with these interactions. Thus, the first response of the immune system against a BoHV-1 infection will consist of nonspecific inflammatory and cell-mediated reactions, gD and gB being primary targets for NK-cells [57]. The innate responses lead to adaptive immune responses later during infection. Glycoproteins gC and gD are targets for CD8+ CTLs in bovines, and gD possesses specific epitopes which stimulate CD4+ T-lymphocytes [58]. Antibody responses, as mentioned, do not prevent cell-to-cell spread and become detectable when recovery from primary infection is underway. Felsenstein, http://evolution.genetics.washington.edu/phylip.html). Non-neutralizing antibodies may also contribute together with PMNs, which can cause lysis of BoHV-1 infected cells via antibody-dependent cell cytotoxicity (ADCC) [59].

Thus, it becomes clear that the major glycoproteins are not only involved in inducing antibody that may protect the animal from disease, but also in stimulating cell-mediated responses, as they are also targets for CTLs and ADCC. For these reasons, it is important that new vaccine strategies against BoHV-1 and -5 focus on or include the major glycoproteins, in particular gD (reviewed in [21]).

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