Grail et al. The genomic organization of both of these FeHV-1 strains was found to be similar to that of other varicelloviruses. We recently reported the first complete genomic sequence of FeHV-1, as well as the construction and characterization of a BAC clone containing the entire viral genome. A total of 78 open reading frames were predicted, encoding 74 distinct proteins.
The gene arrangement was found to be colinear with that of most other varicelloviruses whose genomes have been sequenced [ 14 ]. All alphaherpesviruses are considered to have a replication pattern that is similar to the one of HSV-1 [ 6 , 7 ].
FeHV-1 has previously been shown to contain 23 virion-associated proteins [ 15 ]. The examination of the recently derived complete sequence showed that the FeHV-1 genome in fact contains a total of 13 envelope glycoproteins [ 14 ]. Most studies on the function of FeHV-1 genes have been focused on the role of envelope glycoproteins [ 16 ], because of their predicted role in inducing protective host immune responses and, therefore, their potential for vaccine development.
FeHV-1 typically affects kittens and juvenile cats. Most kittens are protected by passive immunity until they are about 2 months of age. The pathogenesis of FHV-1 is based upon two different mechanisms. The first is that FeHV-1 is a cytolytic virus. Examples of its cytolytic effects are ulcerations in mucosae and the cornea. The second mechanism is immune-mediated, clinically manifesting itself as stromal keratitis. An important question related to this second pathogenetic mechanism is the source of the antigenic stimulation driving this reaction [ 17 ].
The main sources of FeHV-1 transmission are oronasal and ocular secretions from acutely infected cats. Viral transmission can also be associated with the reactivation of latency. Kittens with residual passive immunity may not show clinical signs when exposed but become latently infected [ 18 ]. Following entry via the oronasal route, FeHV-1 replicates extensively in the mucosae of the upper respiratory tract and generally causes severe upper respiratory disease in susceptible animals.
The incubation period varies from 2 to 6 days. The primary replication sites of FeHV-1 include the mucosae of the nasal septum, turbinate, nasopharynx, conjunctivae, and upper trachea. Replication also takes place in tonsils and mandibular lymph nodes. Acute respiratory FeHV-1 infection is characterized initially by fever, inappetence, and sneezing, followed by serous nasal discharge, which can become mucopurulent after 5—7 days.
In addition, oral replication of the virus can result in excessive salivation and drooling of saliva. Occasionally coughing and dyspnea may occur. Oral ulceration, a typical feature of feline calicivirus infection, may occur as a result of FeHV-1 infection of the oral cavity but is uncommon [ 3 ]. The ocular manifestations associated with FeHV-1 infection have been reviewed by Gould [ 5 ]. In neonatal kittens ophthalmia neonatorum has been described and can lead to serious corneal damage.
Acute hyperemic conjunctivitis, leading to ocular discharge and chemosis, a feature of acute infection, occurs in association with upper respiratory signs. The formation of branched epithelial ulcers, referred to as dendritic ulceration, is a pathognomonic feature of acute ocular FeHV-1 infection.
Both dendritic and geographic corneal ulceration may also result from latency reactivation. FeHV-1 is primarily an upper respiratory and ocular pathogen, with only sporadic involvement of the lungs. Viremia levels are low, thought to be related to the natural temperature sensitivity of this virus, which would favor replication in the upper respiratory tract.
Exposure of pregnant queens can lead to abortion, but infection with FeHV-1 infection is not a common cause of abortion in cats. In neonatal kittens, the infection can generalize and is associated with neurological signs and a high mortality rate. A hallmark of alphaherpesvirus biology is that acute infection is followed by lifelong persistence of the viral genome in latent form in nervous and lymphoid tissues. Latency and periodic reactivation of latency are integral parts of the lifecycle of alphaherpesviruses and important elements in their survival and transmission.
The latency-reactivation cycle operationally consists of three major steps: establishment, maintenance, and reactivation. The establishment of latency by definition requires that the virus reaches the tissue in which latency will be established. This process starts during the acute phase of viral replication at peripheral mucosal sites. Nerve endings of sensory nerves innervating viral replication sites take up viral particles and subparticles during this phase. These particles are transported within the axoplasm of the axons of these nerves by a process referred to as retrograde axonal transport.
When the virus reaches the sensory ganglia, it infects neurons and other cell types. This acute infection of ganglionic cell types lasts for approximately one week. Neurons are the cell type in which latency is established. In order to accomplish this, lytic gene expression is repressed, while the latency-associated transcript LAT is expressed, which yields several RNA species by splicing. These multiple species are collectively referred to as LATs. Low level or sporadic transcription of immediate-early and early genes can occur but is not sufficient to initiate a productive infection.
No infectious virions can be detected in the ganglia during latent infection. During the maintenance phase of latency, the viral DNA is present in the neurons in an episomal form. The viral DNA is not totally static during the maintenance phase of latency, but transcriptional activity of the genome is limited to a region referred to as the latency-associated transcript or LAT. The maintenance phase of latency is reversible.
In other words, under the influence of certain natural or pharmacological stimuli, the reactivation of latent viral DNA can occur. Infectious virus can be detected again by virus isolation or PCR from nasal, oral, or ocular swabs. Usually the clinical signs associated with the reactivation process are significantly milder than those seen during the primary infection, and reactivation can certainly be asymptomatic.
Virus shedding resulting from reactivation is also typically at a lower level and of shorter duration than seen during primary infection. However, reactivating virus can still be a significant source of exposure and primary disease in fully susceptible hosts that are in close contact with the animal in which reactivation took place.
Reactivation occurs in only a small subset of latently infected neurons, typically less than 0. Latently infected neurons in which reactivation took place do not survive. This explains why sensory deficits are not associated with reactivation in sensory nerve ganglia. Since the reservoir of latently infected neurons remains large under these conditions, repeated reactivation can take place throughout the life of the host.
Our current understanding of the regulation of latency is derived primarily from studies on HSV-1 and BoHV-1 [ 20 — 22 ]. The following summary is derived primarily from an excellent very recent review of HSV-1 latency by Perng and Jones [ 20 ].
Acute infection of trigeminal ganglia neurons produces toxic gene expression products that make them vulnerable to damage and death. In addition, cellular DNA damage induced by viral replication stimulates the mitochondrial pathway of apoptosis.
Herpesviruses try to counteract apoptosis and thus enhance their replicative ability, by encoding several antiapoptotic genes, one of which is the LAT gene. Since there is redundancy in the viral antiapoptotic capabilities during the acute phase, apoptosis of neurons during this phase is prevented fairly efficiently.
It is very important that apoptosis is prevented also during the establishment and maintenance stage of latency. This is especially crucial in permissive neurons, in which extensive viral replication has taken place during the acute phase.
A mechanism by which LAT-encoded miRNA regulates apoptosis is targeting of transforming growth factor beta, a potent inducer of apoptosis [ 23 , 24 ]. It is important to understand the interactions between the latent viral genome and the neuron that lead to reactivation, because this is a prerequisite to ultimately controlling this process.
LAT plays an important role in the in vivo reactivation of latency. In experimental studies it has been shown that spontaneous reactivation is severely impaired if the LAT gene is deleted. Thompson et al. Prior to establishment of latency virus replication takes place in permissive neurons.
In susceptible cells at mucosal surfaces VP16, a component of virions entering the cell, combined with cellular factors, activates the immediate early genes.
Axonal transport of VP16 into neurons is inefficient, which would promote latency. In order for VP16 to initiate lytic infection, it needs to be synthesized de novo , a process which requires that neuronal inhibition be overcome.
Very interestingly, the LAT locus is considered to express riboregulators that mediate synthesis of VP It has been shown that, in the absence of LAT transcription, half of the neurons destined to be latently infected instead enter the lytic cycle and die.
In contrast when repression is overcome, neurons become lytically infected, and the infectious virus produced spreads both within the ganglia and back to the mucosal surface where infection was initiated.
The goal of lytic infection is to increase the number of latently infected cells. Stress, leading to reactivation, is hypothesized to increase the novo production of VP16 by a mechanism that is still under investigation. The VP16 produced then initiates a feedback loop with the IE genes and results in viral reactivation in a very limited number of latently infected neurons.
Viral antigen production in trigeminal ganglia increases until 3 days after infection but is no longer detectable at 7 days after infection. Persistence of immune effector cells in trigeminal ganglia TG implies that low levels of viral proteins are expressed and that an immune response occurs.
In a mouse HSV-1 model, it has been demonstrated that viral DNA replication, transcription, and viral protein production take place in 1 neuron per 10 TG. Two mechanisms by which these infiltrating cells prevent reactivation are the production of gamma interferon and lymphocyte-mediated cytotoxicity. The trigeminal ganglion is considered a primary site of latency for FeHV-1 although recent studies implied other tissues as potential sites [ 26 , 27 ].
Spontaneous reactivation is possible but does not occur frequently. More commonly leading to the reactivation of latent FeHV-1 is the result of environmental or physiological stresses, such as changes in housing or lactation. The lag phase between the stressor leading to reactivation and the actual shedding of infectious virus is about 4—11 days, and virus excretion lasts for approximately 6 days on average.
Virus excretion by cats in which a reactivation event took place ranges from 1—13 days [ 29 , 31 ]. During this time infectious virus can be demonstrated in ocular and oronasal secretions. The reactivation can be either asymptomatic or associated with clinical signs.
Symptomatic reactivation is referred to as recrudescence. Reactivation of latent viral DNA in adult cats can lead to corneal ulceration, accompanied by varying degrees of conjunctivitis [ 32 ]. Since herpetic stromal keratitis caused by HSV-1 is the leading cause of infectious blindness in industrialized countries, ocular infection of FeHV-1 in cats is considered a very good natural host model.
Infectious virus is carried by anterograde axonal transport to peripheral tissues, usually to cells at or near the site of initial infection, and is a potential source of viral transmission [ 6 , 7 ]. The role of reactivation in the epidemiology of alphaherpesviruses is directly related to the frequency by which it takes place. Some herpesviruses, including FeHV-1, reactivate much more easily than others from the latent state, both under natural and experimental conditions.
The ease by which latent FeHV-1 DNA is reactivated is an important element in the justification of FeHV-1 infection of cats as a natural host model to study the molecular pathogenesis of herpesvirus latency and approaches to prevent it. Clinically, there is an overlap between the symptomatology of acute FeHV-1 and feline calicivirus FCV , another major respiratory disease of cats. Distinguishing features of FeHV-1 infection are high fever and corneal ulcerations. In contrast, ulcers of the tongue, palate, and pharynx are more typical or encountered more frequently in calicivirus infections.
The most common laboratory diagnostic methods to demonstrate the presence of FeHV-1 or viral components in tissue homogenates or swabs include the direct fluorescent antibody FA test, virus isolation VI , and PCR [ 3 , 5 , 18 ].
Fluorescent antibody testing is performed on conjunctival or corneal tissue. This test is far less commonly used now than it used to be. Topical fluorescein, used to visualize ulcers, should be avoided prior to collecting samples. Laboratory diagnosis of acute FeHV-1 is now most commonly performed by virus isolation VI or PCR, using oronasal and conjunctival swab extracts as the samples.
VI detects infectious virus and has been the laboratory diagnostic gold standard [ 4 , 28 ]. The assay was determined to be very specific for FeHV-1, and its detection limit was between 0. Infectious virus titers and viral DNA correlated over a wide dilution range. Early during infection, referred to as phase 1, the correlation between virus titers and qPCR signals was very high. Next, during so called phase 2, a rapid decline in infectious virus titers was seen, while the qPCR signals remained high.
During the final phase, referred to as phase 3, infectious virus was no longer detectable, and the quantitative PCR signals were also declining. Analysis of the combined virus detection and qPCR results on 20 clinical samples allowed the authors to reliably define the phase of the infection during which the samples had been collected.
Realizing the cost of combined testing, it was suggested to test consecutive samples by qPCR to accomplish this goal. Maggs [ 4 ] pointed out 3 aspects of laboratory diagnosis of FeHV-1 that can be very frustrating for the clinician. Whereas the confirmation of acute FeHV-1 is not always required, it is important to confirm that chronic lesions are caused by FeHV Unfortunately, the detection of FeHV-1 or viral components in these lesions can be difficult.
The second aspect of laboratory diagnosis that leads to misinterpretations is the fact that FEHV-1 or viral l DNA can be detected in samples from clinically normal cats. It was pointed out that the detection of FeHV-1 or its components can be coincidental, consequential, or causal. Differentiating between these possibilities is obviously important.
Virus neutralizing antibody titers are determined by VN tests, which are commonly used to detect prior infection or the efficacy of vaccination. Virus neutralizing antibodies can be low and slow to develop. As pointed out by Dawson et al. Pin On Cats Health Problems. Herpesvirus And The Feline Eye. Aza Blessed from west Africa He is one of the oldest herbalist after Dr.
Post a Comment. Holistic Treatment Of Feline Herpesvirus. January 10, Here we provide a variety of interesting information or pictures Holistic treatment of feline herpesvirus Bronchiseptica infection in cats.
Feline Herpesvirus Natural Treatment No Lysine It requires a thorough examination several prescriptions and repeated evaluations if you.
Popular posts from this blog Mingus The Panther September 11, Are you looking for information or pictures about Mingus the panther. Here we provide a variety of interesting information or pictures Mingus the panther The Bombay cat is a type of short-haired cat developed by breeding sable Burmese and black American Shorthair cats to produce a cat of mostly Burmese type but with a sleek panther -like black coat.
Since Mingus has outscored the Panthers and was a perfect in that time span before Friday nights debacle. Mingus the panther. When the opportunity arises to win a prestigious scholarship she seeks out a letter of recommendation from the most popular faculty member on campus Harrison. But theyre not theyre just his teeth Several years ago Nicole Rienzie was driving with her mom when a black kitten darted in front of her car.
A black. Read more. November 01, Airway Collapse. Canine Hypothyroidism. Cranial Cruciate Injury. Elbow Osteoarthritis. Feline Herpesvirus. Immune-Mediated Hemolytic Anemia Treatment. Pulmonary Hypertension. Itching Dog. Tracheal Collapse.
Urine Spraying in Cats. Vestibular Disease. Localising Lesions: Brain. Localising Lesions: Spinal Cord. Practical Seizure Management. Disorders of Peripheral Nervous System.
Craniocervical Malformations. Spinal Surgery. Surgical Disorders of Brain. Blood Glucose Curves. Constant-Rate Infusions. Insulin Preparations. Difficult Pain Cases. Medical Therapy of CHF. Open Wound Management. Oral Pathology. Postoperative Care. Faecal Exam. Reducing Stress for Cats. Dietary Management of GI Disorders. Hydrolysed Protein Diets. Nutrition of Hospitalized Patient. Nutrition for Senior Pets. Feeding Pets. Oncologic Surgery. Predicting Cancer Behaviour. Reconstructive Surgery.
Soft-Tissue Sarcoma. Surgical Planning for Cancer. Chemotherapy Drugs. Bladder Matters. Cutting Edge Treatments. Molecular-Targeting Therapy. Antibiotic-Resistant Bacteria. Leptospirosis in New Zealand. Zoonoses, Emerging Infectious Disease. Complete Ocular Examination. Red Eyes. Glaucoma Management.
Cool Eye Cases. Eye as Indicator for Systemic Disease. Ocular Injuries. Herpes Virus-1 Ocular Disease. Corneal Ulcer Management. When Eyes Get Blues. Transdermal Administration. Empirical Antibiotic Therapy. Feline Therapeutics. If not treated, the cat can run a fever and may have a loss of appetite. They may show no desire to drink water, either. Dehydration can be an issue that sets in and this can be quickly fatal in cats.
This illness is most prevalent in cats that are stressed out. However, it can affect other cats as well. This is understandable because feline herpes affects the immune system.
This is one of the biggest issues since it can allow secondary infections that can be fatal. However, it is treatable. A vet should be consulted, but the sickness is treated with L-lysine. This gives the cat a boost to the immune system. L-lysine is an amino acid and it is available over the counter at many health food stores and pharmacies.
This amino acid is also used in the treatment of herpes or cold sores in humans.
0コメント