bovine immunodeficiency virus infection
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- bovine immunodeficiency virus infection
Other Scientific Names
- bovine visna virus infection
International Common Names
- English: BIV infection; bovine immunodeficiency-like virus; bovine lentivirus infection, bovine immunodeficiency virus, biv; bovine viral immunodeficiency syndrome
- Spanish: sindrome de inmunodeficiencia viral bovina
Pathogen/sTop of page
OverviewTop of page
Bovine immunodeficiency virus (BIV) is a lentivirus that was first isolated in the USA from a Holstein dairy cow with lymphoproliferative lesions during an investigation of the aetiology of enzootic bovine leukosis (Van der Maaten et al., 1972), and was originally termed ‘bovine visna virus’ due to its similarities to the eponymous sheep virus. The discovery of human immunodeficiency virus (HIV) led to an increased interest in lentiviruses and further characterisation of BIV (Gonda et al., 1987). Infection with BIV has been shown to be associated with lymphadenopathy, lymphocytosis, ataxia, encephalitis, weakness and emaciation (Van der Maaten et al., 1972; Carpenter et al., 1992; Snider et al., 1996; Munro et al., 1998) but it is still controversial as to whether BIV causes true immunodeficiency. Indeed, BIV has also been called ‘bovine immunodeficiency-like virus’, reflecting this uncertainty.
Serological data suggest that BIV occurs throughout the world with the highest prevalence in the USA and Canada, where estimates of the prevalence of infection range from 20 to 60%. Seroepidemiological evidence has been presented for other countries in Europe and Japan, suggesting that the prevalence there is much lower, at 4-35%. The impact of BIV infection on disease in cattle is also controversial. In some cattle herds in the southern USA, BIV has been cited as the underlying cause of a syndrome of ill health and poor performance (Gonda et al., 1994; McNab et al., 1994; Snider et al., 1996, 1997) while other reports provide little evidence of pathogenicity (Martin et al., 1991; Onuma et al., 1992; Flaming et al., 1993; Suarez et al., 1993). There is considerable interest, therefore, in establishing the role of BIV in cattle disease. The majority of naturally acquired infections fail to produce a specific clinically recognised syndrome. Infection with BIV may predispose cattle to an increased incidence or severity of endemic diseases.
Host AnimalsTop of page
Hosts/Species AffectedTop of page
BIV appears to be specific for infection of its natural host Bos taurus. Sheep, goats and rabbits have been experimentally infected with cell-associated virus but in the field there is no evidence of natural infection (Whetstone et al., 1991; Pifat et al., 1992; Jacobs et al., 1996, Kalvatchev et al., 1998). A transient viraemia was detected following experimental infection of Bali cattle with BIV, together with a variable antibody response, but there were no clinical signs of disease (McNab et al., 2010). It does appear that rodents are not susceptible to BIV infection (Gonda, 1992). These findings support evidence that lentiviruses are species-specific.
Systems AffectedTop of page
nervous system diseases of large ruminants
DistributionTop of page
Serological evidence shows BIV infection to be worldwide but virus isolation in many cases has proved elusive. It has been suggested that there is a higher prevalence in cattle from the southern USA than from the northern states. Despite this high seroprevalence, only a few isolates are available for study, the original R29 isolate and two that have been isolated from cattle in Florida (Suarez et al., 1993). BIV may also be present in cattle in Portugal, Switzerland, Croatia, and the UK; it is possible that the absence of confirmed reports of BIV infection in some countries is due to the unavailability of a suitable diagnostic test and lack of investigation.
A second lentivirus of cattle, Jembrana Disease Virus, has also been isolated but is restricted to Indonesia (Chadwick et al., 1995). This virus is antigenically and genetically closely related to BIV (Kertayadnya et al., 1993) but causes acute disease in Bali cattle (Bos javanicus) (Dharma et al., 1991) and a much milder syndrome in Bos taurus (Suarez et al., 1993).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Japan||Present||Present based on regional distribution.|
|Canada||Present||Present based on regional distribution.|
PathologyTop of page
BIV strain R29 was originally isolated from an animal that presented at necropsy with a generalised hyperplasia of the lymph nodes and a mild perivascular cuffing in the brain (van der Maaten et al., 1972); however, it is considered that clinically detectable lymphadenopathy and active BIV infection of the brain are not generalised features of BIV infection. Recent experimental studies have shown an association of BIV infection with lymphadenopathy and non-suppurative meningoencephalitis (Munro et al., 1998). The most common finding on post mortem examination of BIV infected animals was enlarged spheroidal, black coloured haemal nodes found associated with or encapsulated within the other carcass lymph nodes (Van der Maaten et al., 1972; Munro et al., 1998). Size, number and distribution of these nodes varied between animals. Histological evidence of meningoencephalitis has been demonstrated (Munro et al., 1998) and BIV has been detected in the brains of infected animals by PCR (Snider et al., 1996).
There is still uncertainty over the pathological effects of BIV infection and it should be remembered that the tissue-culture adapted R29 isolate used in most experimental infections may have become attenuated over the years and may not be directly comparable to either natural infection or experimental infection with the more recent Florida isolates.
In BIV infected cattle, proviral DNA has been detected by PCR and in-situ hybridisation in many tissues (Zhang et al., 1997a; Carpenter et al., 1992; Lew et al., 2004; Heaton et al., 1998; Wu et al., 2003; Baron et al., 1998). Reports have suggested that the predominant in vivo targets for BIV are cells of the monocyte/macrophage and B cell lineages (Carpenter et al., 1992; Onuma et al., 1992; Pifat et al., 1992; Heaton et al., 1998). Recent studies with new isolates and molecular techniques suggest that BIV may be pan-tropic (Whetstone et al., 1997; Heaton et al., 1998; Wu et al., 2003).
DiagnosisTop of page
Clinical diagnosis of BIV infection is rarely possible. One of the difficulties in assessing the role of BIV in bovine disease is the inconsistency of methods to detect infected cattle and the variable immune responses that accompany many lentiviral infections. While sero-epidemiological surveys have demonstrated that BIV infection occurs in many parts of the world, some of the assays used are unreliable and may have given false positive results. In addition, in certain assays the antibody response to some BIV antigens appears to decline to undetectable levels within a few months of infection (Isaacson et al., 1995) so that false negative results may be obtained. There is thus an urgent requirement for a reliable assay to specifically detect antibodies to BIV which can be used to study the immune response of cattle to infection and to investigate the occurrence of infection in cattle populations where the prevalence has been reported to be low (Horzinek et al., 1991). Another problem is that all assays are based on the only two available BIV strains, R29 and FL112. This raises the issue that some strains present in the field may be missed due to antigenic differences between field strains and the virus used as a source of antigen in the diagnostic tests. For this purpose, an assay that could detect antibodies to all BIV strains would be essential.
Many different tests have been reported for diagnosis of BIV (last reviewed in Evermann and Jackson, 1997). Most are based on serology utilising indirect immunofluorescent antibody (IFA) (Amborski et al., 1989; Whetstone et al., 1990), western blot (Whetstone et al., 1991; Abed et al., 1999) and ELISA technology (Scobie et al., 1999; Abed and Archambault, 2000). Diagnosis using PCR is also successful in confirming the presence of proviral DNA (Zhang et al., 1997a; Suarez and Whetstone, 1998) and sensitive qPCR methods have been developed recently (Lew et al., 2004). Virus isolation in cell culture is of limited use as it can be complicated by the presence of other viral agents and has very low sensitivity. IFA is not widely used due to potential problems with cross-reacting viruses and sensitivity, and it is unsuitable for screening large numbers of field samples. A Bayesian comparison of antibody detection using IFA versus nested PCR for the detection of BIV proviral DNA concluded that although PCR was more sensitive, substantial misclassification of infection was likely irrespective of the detection method used (Orr et al., 2003).
Although PCR is relatively expensive and requires further purification steps to obtain suitable samples, it has the advantage of being both extremely sensitive and specific. The development of qPCR assays to detect BIV proviral DNA (Lew et al., 2004) offer significant improvements over the nested PCR assays that have been used previously and can be used for high throughput screening of samples.
The most likely candidate for an inexpensive and relatively simple method for screening large populations is an ELISA. This requires a sample of blood and the serum can be tested for the presence of BIV antibodies. Antigens have been developed based on the p26 and TM regions of BIV and incorporated into ELISA tests, which have been confirmed using western blot. A competitive inhibition ELISA using a recombinant capsid specific antibody has recently been developed and is reported to offer increased sensitivity (Bhatia et al., 2010). The TM antigen appears to be immunodominant so that a higher proportion of cattle have antibodies to TM than to other viral proteins (Chen and Frankel, 1994; Abed et al., 1999; Abed and Archambault, 2000). There also appears to be no cross-reactivity with TM and other common bovine viruses and a peptide ELISA has been successfully developed based on the immunodominant domain of this protein (Abed and Archambault, 2000; Scobie et al., 1999).
List of Symptoms/SignsTop of page
|General Signs / Ataxia, incoordination, staggering, falling||Cattle & Buffaloes|All Stages||Sign|
|General Signs / Generalized lameness or stiffness, limping||Cattle & Buffaloes|All Stages||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Cattle & Buffaloes|All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Cattle & Buffaloes|All Stages||Sign|
|General Signs / Weight loss||Cattle & Buffaloes|All Stages||Sign|
|Nervous Signs / Abnormal behavior, aggression, changing habits||Cattle & Buffaloes|All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Cattle & Buffaloes|All Stages||Sign|
|Nervous Signs / Hyperesthesia, irritable, hyperactive||Cattle & Buffaloes|All Stages||Sign|
|Ophthalmology Signs / Prolapsed third eyelid, protrusion nictitating membrane||Cattle & Buffaloes|All Stages||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Cattle & Buffaloes|Cow||Sign|
Disease CourseTop of page
The progress of the disease has been difficult to assess. Experimentally, cattle become seropositive for BIV by 2-4 weeks after infection (Venables et al., 1997; Scobie et al., 1999) and maintain an antibody response to the major proteins of the virus for longer than 2 years, although antibody to the Gag proteins has been demonstrated to decline within this period (Isaacson et al., 1995). Long term persistence does not appear to result in selection pressure and emergence of new serological strains of virus. Proviral DNA has also been detected by PCR at these early stages (Suarez et al., 1995; Venables et al., 1997; Suarez and Whetstone, 1998).
Observations of the development of clinical disease have varied between workers and the pathogenicity of BIV remains controversial. Many varying signs have been recorded which are not consistent. The most common reported signs are lymphadenopathy, weakness and emaciation. Generalised lameness and ataxia have also been evident (Snider et al., 1997; Munro et al., 1998) and some workers have reported a fall in milk yield (McNab et al., 1994). However, most animals found to be seropositive for BIV have no clinical signs.
In experimentally infected animals, there is some evidence of abnormal behaviour and aggression, which has not been reported for naturally infected cattle. Signs also appear to vary between individual cattle with some demonstrating hyperactivity while others becoming dull and listless.
The potential for BIV to dysregulate the immune system has been widely recognised, but again conclusive evidence of this has yet to be established. Immunosuppression in cattle may result from exposure to a number of infectious or toxic agents. There has been suggestion that dual infection of bovine leukaemia virus (BLV), and BIV occurs (Hidalgo et al., 1995; St Cyr Coats, 1995), but reports from other sources have found no correlation with seropositivity of animals (Cockerell et al. 1992; Hirai et al., 1996). Liang et al. (1995) and Liu et al. (1997b) demonstrated that BVD and BHV respectively can result in the in vitro transactivation of BIV and a potential role for BIV in bovine paraplegic syndrome has also been suggested (Walder et al., 1995). Investigation of the co-operation between BIV and other widespread cattle viruses should be considered, to ensure that cattle infected with BIV do not present a significant risk to other cattle within a herd.
During outbreaks of common diseases of cattle including pneumonia, diarrhoea and abortion, farm animal clinicians may find it difficult to explain why some individuals are affected by disease while others are not, or why some individuals are much more severely affected than others. This is particularly the case when cattle are kept in the same environment and are often of similar genetic background. Cattle from herds with these particular problems should be screened to establish if BIV might be an underlying cause.
EpidemiologyTop of page
The viral life cycle follows the natural progression as described for HIV (reviewed by Gonda, 1994). Once infected, animals have a persistent and chronic lifelong infection; however, the period of development for natural infection is unclear.
How BIV is transmitted between animals has not been fully established although transmission is thought to be horizontal, as for the other lentiviruses. BIV proviral DNA has been detected in the blood and semen of experimentally infected bulls (Gradil et al., 1999) as determined by indirect immunofluorescent antibody (IFA) testing and/or PCR. Jacobs et al. (1998) found that 12.6% of bulls tested by PCR were positive as compared to only 9.6% when serology was used. Both studies demonstrate the presence of BIV in both blood and semen but do not prove that infectious virus was present or whether transmission can occur through breeding practices.
Scholl et al. (2000) demonstrated that transplacental BIV infection can occur between seropositive dams and their calves. The effect of prenatal BIV infection on the health of the neonates was not indicated. There is also a potential for lactogenic transmission as BIV has been isolated from leukocytes derived from milk (Nash et al., 1995). However this risk could be minimised by the inactivation of BIV in milk and colostrum before hand feeding to calves (Moore et al., 1996). One of the most likely methods of the spread of infection is iatrogenically by the mass inoculation of cattle with shared needles during multiple vaccinations. There is no evidence to support the probability that BIV present in vector hosts would lead to amplification or biological transmission.
Impact: EconomicTop of page
The economic importance of the bovine immunodeficiency virus cannot be truly assessed until the nature of the disease associated with BIV infection is understood. It is difficult to define whether the virus per se is significantly detrimental to cattle health or if it predisposes the animal to opportunistic infection with other cattle pathogens. Research into dual infection with other diseases such as BVD and BLV may provide information to answer these questions. The financial loss attributable to BIV infection is unknown.
Zoonoses and Food SafetyTop of page
There is no evidence to suggest that BIV presents a significant risk to man as infection has only been reported in Bos taurus. A number of laboratory workers exposed to the virus did not seroconvert (Whetstone et al., 1992).
Lentiviruses are heat labile; the virus is inactivated and rendered safe by the pasteurisation of milk (Venables et al., 1997), and by treatment at lower temperatures (Moore et al., 1996). MacDiarmid (1992) has suggested that BIV constitutes no threat to human health due to its inability to survive the processing and storage methods associated with trade and dairy products. No evidence of transfer of infection by human consumption of cattle products has been reported.
Disease TreatmentTop of page
Symptomatic treatment of secondary infections is the only treatment method available at present.
Prevention and ControlTop of page
It has been suggested that clinical disease can be associated with stress. Snider et al. (1997) monitored experimentally infected dairy and beef herds and suggested that clinical signs were more apparent in BIV infected dairy cattle than in beef cattle, possibly due to lower stress factors in beef cattle production. Some of the more common stress factors linked to disease appear to be temperature extremes, parturition, feeding practices and over-crowded housing. Unfortunately, modern farming methods make it difficult to eliminate these factors.
In cases where herds naturally infected with BIV have been identified, management deficiencies such as poor nutrition, inadequate housing and poor husbandry have been found (Snider et al., 1997). Improvements in cattle management can be monitored and farmers can be advised on animal welfare.
Restrictions on the import and export of BIV-infected cattle cannot be justified unless certain constraints are overcome. A sensitive and accurate diagnostic method would have to be in place, as would a state-run programme for the control and prevention of spread of the disease. Evidence from serological studies suggests that the prevalence in continental Europe and the UK is similar and that continuing movement of animals using current methods would not alter this status significantly.
Until a specific disease syndrome is associated with BIV infection, it is questionable whether the infection requires to be controlled. There are currently no methods to prevent infection and vaccine development has not been undertaken due to the lack of pathogenicity of the virus and its questionable economic impact on infected cattle.
ReferencesTop of page
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