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EPIDEMIOLOGY OF NATURAL TRANSMISSION
OF BOVINE LEUKEMIA VIRUS INFECTION



BY



MARK CY THURMOND



A DISSERTATION PRESENTED TO THE GRADUATE COUNCIL

OF THE UNIVERSITY OF FLORIDA IN PARTIAL

FULFILLMENT OF THE REQUIREMENTS FOR

THE DEGREE OF DOCTOR OF PHILOSOPHY



UNIVERSITY OF FLORIDA
1982



Copyright 1982



by



Mark Cy Thurmond



DEDICATED TO
AUDREY



ACKNOWLEDGEMENTS

Technical assistance with agar-gel immunodiffusion and
animal sampling was provided by Ms . J. Hennemann, Ms. J.
Ring, Mr. C. Maden, Mr. T. O'Donnell, Mr. A. Green, and
Mr. J. Lindsey. Most data management and computer program-
ming were performed by Ms. J. Galvez and Mr. D. Puhr . Edi-
torial assistance was provided by Dr. M. Burridge, Dr. P.
Nicoletti, and Dr. C. Wilcox. The typist was Ms. B.
Smerage. The valuable support and discussions offered by
the following people are gratefully acknowledged: Dr. M.
Burridge, Dr. R. Carter, Dr. M. Drost, Dr. C. Franti
(University of California/Davis), Dr. J. Gaskin, Dr. R.
Kahrs, Dr. J. Miller (USDA, Ames, lA) , Dr. K. Portier,
Dr. 0. Straub (West Germany), Dr. M. Van Der Maaten (USDA,
Ames, lA) , Dr. S. Walter (Yale University), and Dr. C.
Wilcox. Additional thanks is extended to Dr. R. Carter,
Dr. K. Portier, and Dr. C. Wilcox for their interest and
support in statistical designs and analyses. Financial aid
was provided by United States Department of Agriculture
cooperative agreement 58-519B-0-872 and by the Wetterburg
Foundation of Newark, New Jersey.



TABLE OF CONTENTS

PAGE

ACKNOWLEDGEMENTS iv

ABSTRACT viii

CHAPTER

I INTRODUCTION 1

II LITERATURE REVIEW .... 4

Bovine Leukemia Virus Infection 4

Bovine Leukemia Virus 5

Pathogenesis 6

Transmission Via Excretions and

Secretions 8

Serology 9

Factors Examined for Associations with

Bovine Leukemia Virus Infection .... 9
Transmission of Bovine Leukemia Virus

Infection 13

Infection in Other Domestic Animals. ... 16

Reviews 17

III GENERAL MATERIALS AND METHODS 18

Population Studied 18

Location and Climate 18

Management Practices 18

Sampling Design 22

Demographic Information 2 3

Serology 24

Other Species Examined 25

Diseases or Conditions Observed 25

Data Collection and Computer Programs. . . 26

IV IN UTERO TRANSMISSION OF BOVINE LEUKEMIA

VIRUS 27

Introduction 27

Materials and Methods 28

Results 29

Discussion 31



PAGE

V DECAY OF COLOSTRAL ANTIBODIES TO BOVINE

LEUKEMIA VIRUS 41

Introduction 41

Materials and Methods 41

Results 44

Discussion 45

VI AGE-SPECIFIC RATES OF DETECTION OF BOVINE

LEUKEMIA VIRUS INFECTION 53

Introduction 53

Materials and Methods 54

Results 58

Discussion 60

VII SEASONAL PATTERNS OF RATES OF BOVINE

LEUKEMIA VIRUS INFECTION 8 3

Introduction 83

Materials and Methods 84

Results 86

Discussion 87

VIII SPATIAL PATTERNS OF BOVINE LEUKEMIA VIRUS

INFECTION 98

Introduction 98

Materials and Methods 99

Results 104

Discussion 105

IX IATROGENIC TRANSMISSION OF BOVINE LEUKEMIA

VIRUS INFECTION 118

Introduction 118

Materials and Methods 118

Results 120

Discussion 120

X SUMMARY 129

APPENDICES

A PLAT OF THE UNIVERSITY OF FLORIDA DAIRY

RESEARCH UNIT 134

B AVERAGE MONTHLY HIGH AND LOW TEMPERATURES
AND RAINFALL BETWEEN JULY 1, 1979, AND
SEPTEMBER 30, 1981, FOR GAINESVILLE,

FLORIDA 135



PAGE

C MONTHLY FREQUENCIES OF CALVES BORN ALIVE

BETWEEN JULY 1, 1979, AND JUNE 30, 1981,

AT THE UNIVERSITY OF FLORIDA DAIRY

RESEARCH UNIT 136

D LOCATION SITES AT THE DAIRY RESEARCH UNIT . , 137

E PRECIPITATION LINES OF AGAR-GEL IMMUNO-
DIFFUSION 144

LIST OF REFERENCES 145

BIOGRAPHICAL SKETCH 166



Abstract of Dissertation Presented to the Graduate Council

of the University of Florida in Partial Fulfillment of the

Requirements for the Degree of Doctor of Philosophy



EPIDEMIOLOGY OF NATURAL TRANSMISSION
OF BOVINE LEUKEMIA VIRUS INFECTION

by

Mark Cy Thurmond

May 1982

Chairman: Michael Burridge
Major Department: Animal Science

A 27-month study examined 473 dairy cattle for associa-
tions between bovine leukemia virus (BLV) infection and host
and environmental factors. Cattle sera were tested at
monthly intervals for BLV antibodies by agar-gel immuno-
diffusion using the glycoprotein-51 antigen. A model of BLV
colostral antibody decay in 130 calves predicted infection
in calves less than six months of age and estimated anti-
body half-life to be 27.1 ±1.2 days. Colostral antibody
decay did not differ between BLV-infected and noninfected
calves for slope (p = 0.45) or intercept (p = 0.43). By 95
days of age, 50% of the calves had no detectable BLV
colostral antibodies.

Of 125 calves born to BLV-infected cows and followed
for at least four months, eight (6.4%) had precolostral BLV
antibodies, as determined by radioimmunoassay using the
glycoprotein-51 antigen- In utero infection with BLV was



not associated with dam age (p = 0.86), dam parity (p = 0.83),
breed (p = 0.66), sex (p = 0.11), or stage of gestation in
which the dam was infected (p=0.50). Calves infected in
utero did not pose an increased risk of infection to calves
penned next to them (p = 0.61).

Prevalence rates of infection were 9%, 16%, and 63% at
6, 16, and 27 months of age, respectively. Age-specific
rates of infection were not associated with dam age (p =
0.79), dam parity (p=0.75), dam BLV-status (p = 0.46), breed
(p = 0.86), or BLV-status of colostrum consumed (p=0.50).

An algorithm was described which allocated probabili-
ties of infection to locations occupied by an animal prior
to detection of infection. Small calf pastures were associ-
ated with less infection than was the calf barn (p< 0.05) .
No less infection was associated with individual outdoor
calf pens compared to contiguous indoor pens (p>0.05).
Risk of infection associated with the dry herd was five
times that for heifer pastures (p< 0.0001) and accounted
24 infections per 100 heifers per 100 days at risk.

Vaccination for infectious diseases was not associ-
ated with increased BLV infection (p=0.33). Infection
rates were not associated with month of birth (p = 0.24) or
with season of potential arthropod vectors (p = 0.20) .
Heifer infection was likely to occur in late v/inter or
spring (p = . 01) .



CHAPTER I
INTRODUCTION



Bovine leukemia virus (BLV) has been shown to be the
causative agent of enzootic bovine leukosis, a neoplastic
disease of cattle (Callahan et al., 1976; Kettmann et al.,
1976; Miller et al., 1969). Bovine leukosis is believed to
have spread to western European countries from the Baltic
region during World War I (Bendixen, 1965) . Following
World War II, efforts were undertaken in some European
countries to reduce the tumor incidence rate through hemato-
logic examinations for persistent lymphocytosis, a phenomenon
associated with bovine lymphosarcoma (Bendixen, 1965).
After discovery of BLV, and subsequent development and use
of serologic methods for mass screening (Hof f-jorgensen et
al., 1978; Miller et al . , 1969; Miller and Van Der Maaten,
1976a; Onuma et al . , 1975; Schmidt et al., 1978), eradica-
tion of enzootic bovine leukosis progressed rapidly (Bause
et al., 1978; Mammerickx et al . , 1978a; Straub, 1978b).

In order to preserve gains made in these programs,
restrictions were placed on BLV-seropositive cattle and on
semen entering countries either free from BLV or with BLV
control programs (Miller, 1980) . Such restrictions have
placed an economic burden on the cattle export markets of
the United States (Mix, 1979) . Because of the high genetic



quality of American cattle, eradication or control of BLV
infection using European methods of test and slaughter
would not be a pragmatic alternative for the American pro-
ducer. Interest, therefore, has focused on prevention of
transmission and test and segregation within a herd (Miller
and Van Der Maaten, 1978a) .

A prerequisite to control of BLV in a herd is a clear
understanding of natural transmission of infection from
fetal life to adulthood or to the age at which heifers
would move to export markets. Several constraints make the
study of natural transmission patterns difficult and may
explain the lack of reports of long-term prospective studies
in the literature. A major obstacle is the necessity for a
large sample of animals to be tested at close intervals
over a long time period. At the same time changes in man-
agement or environmental factors jnust be recorded.

The device used to measure infection must be sensitive,
specific, inexpensive, simple, and meet specifications of
other programs. This necessitates the use of agar-gel im-
munodiffusion because it fulfills the above conditions
(Miller, 1980) . Definition of infection by a serologic
test, however, has important limitations. For instance,
discrimination has not been made between colostral anti-
bodies and infection-induced antibodies in calves less
than six to seven months of age which consumed colostrum
from a BLV-infected cow (Ferrer et al . , 1977b). Another
problem in defining infection is that seroconversion may



lag behind BLV infection by as much as two to three months
(Mammerickx et al., 1980; Straub, 1978b; Van Der Maaten and
Miller, 1978b, 1978c) .

These constraints are not unique to the study of the
epidemiology of BLV transmission. It is important, there-
fore, that designs for the study and eventual control of
BLV be generally applicable to the study of other diseases
and infections.

Examination of risks of BLV infection in a large cattle
population over a 27-month period is presented here as a
logical progression from the fetal environment to adult-
hood. Detection of BLV infection based on serologic cri-
teria is used as a proxy for infection. The intent is not
to attempt statements about specific routes of BLV infec-
tion, but to describe temporal and spatial patterns of
natural infection observed in animals studied. Furthermore,
factors possibly associated with deviations in those pat-
terns will be examined using existing analytic methods in
a framework applicable to other diseases. In addition, new
techniques are presented which improve the efficiency of a
serologically-based diagnosis.



CHAPTER II
LITERATURE REVIEW



Bovine Leukemia Virus Infection



Clinical Appearance

Manifestations of infection with BLV vary from no
signs to persistent lymphocytosis or to lymphosarcoma
(Abramova et al . , 1974; Grimshaw et al . , 197 9; Kenyon and
Piper, 1977; Kumar et al . , 19 78; Sorenson, 1979; Stober,
1968). Clinical signs of tumor involvement usually are
seen in cattle over five years of age and are referable to
the organ system involved (Abramova et al., 1974, Grimshaw
et al., 1979; Sorenson, 1979; Stober, 1968).

Sporadic bovine leukosis (i.e., juvenile, thymic, or
cutaneous leukosis) is not associated with BLV infection
(Bundza et al . , 1980; Chander et al . , 1977; Onuma, 1978;
Onuma et al., 1979; Richards et al . , 1981; Straub and
Weiland, 1977) .

In the absence of tumor involvement, BLV-infected
animals do not appear to suffer production losses (Langston
et al., 1978) .

Distribution

Bovine leukemia virus infection is a ubiquitous infection

throughout the world (Burny et al . , 1980; Burridge et al . ,

4



1981) . A survey of cattle in the state of Florida recently
estimated the infection rate of BLV in dairy cattle to be
48% (Burridge et al . , 1981).

Bovine Leukemia Virus

Discovery of BLV was made following phytohemagglutinin-
stimulation of lymphocytes from cattle with lymphosarcoma
(Miller et al . , 1969). The virus is classifed as a single-
stranded RNA retrovirus (Burny et al . , 1980). It is spheri-
cal in shape with a diameter of 60-125 nm (Calafat et al . ,
1974; Calafat and Ressang, 1977a, 1977b; Dutta et al . ,
1970; Miller et al . , 1969).

Several viral proteins have been described. There are
at least two glycoproteins, gp-30 (Dietzschold et al . ,
1978) and gp-51 (Onuma et al . , 1975), which constitute the
outer shell of BLV (Burny et al . , 1980; Devare and
Stephenson, 1977; Driscoll et al . , 1977). An ether-
resistant protein constitutes the internal or core anti-
gen, known as p-24 (Gilden et al . , 1975; McDonald and
Ferrer, 1976; Miller and Olson, 1972) . The BLV genome
codes for a reverse transcriptase which has a unique re-
quirement for Mg (Dietzschold et al . , 1978; Gilden et
al., 1975; Graves et al . , 1977; Kettmann et al . , 1976).
Six mutant strains of BLV have been investigated recently
(Couez et al . , 1981; Kettmann et al . , 1981).

Several investigators have identified BLV as a C-type
virus (Burny et al . , 1980; Dutta et al . , 1970; Ferrer et al . ,



1971; Kawakami et al . , 1970; Mussgay et al . , 1977; Stock
and Ferrer, 1972; Van Der Maaten et al., 1974; Weiland
and Ueberschar, 1976) . Others have been reluctant to de-
scribe BLV as a B- or C-type virus since immature viruses
are rarely found outside the cell (Calafat et al . , 1974;
Calafat and Ressang, 1977a, 1977b; Dekegel et al . , 1977).

Comparisons of BLV with other retroviruses or onco-
viruses by molecular hybridization have shown that BLV is
biochemically distinct from Friend mouse leukemia virus and
visna maedi virus (Kaaden et al., 1977), Rauscher leukemia
virus (Kettmann et al., 1975, 1976), simian sarcoma (wooly
monkey) virus, murine sarcoma virus, feline sarcoma virus,
and feline leukemia virus (Kettmann et al . , 1975, 1977),
Other studies have demonstrated a lack of cross-reactivity
between proteins of BLV and Mason Pfizer monkey virus
(McDonald and Ferrer, 1976; McDonald et al , 1976), and
bovine syncytia virus (McDonald et al . , 1976).

Pathogenesis

Tissues Involved

Replication of BLV occurs mainly in B-lymphocytes
(Kenyon and Piper, 1977; Paul et al . , 1977), but an associa-
tion with T-lymphocytes also has been reported (Takashima
et al . , 1977). Further support for B-cell involvement was
found in the expansion of the B-cell population in BLV-
infected cattle (Kenyon and Piper, 1977; Kumar et al . ,
1978) .



Following subcutaneous inoculation of leukocytes from
a BLV-infected steer, BLV was isolated from the spleen
after eight days, from leukocytes after 14 days, and oc-
casionally from prescapular lymph nodes thereafter (Van Der
Maaten and Miller, 1978b) . In that study, BLV could be
isolated from lymphocytes two to three weeks before a de-
tectable serologic response, and virus was not isolated
from the thymus. As few as 2500 washed lymphocytes from an
infected steer have been able to transmit BLV infection to
susceptible calves (Van Der Maaten and Miller, 1978c) .

Integration of BLV in the Host Cell Genome

Results of studies using BLV-specific DNA probes sug-
gest that BLV is an exogenous virus (Callahan et al . , 1976;
Deschamps et al . , 1981; Kettmann et al . , 1976, 1978a, 1978b,
1979a; Kukaine et al . , 1979). The DNA from lymphocytes of
BLV-infected cattle has viral sequences that cannot be
identified in the DNA from lymphocytes of noninfected cat-
tle (Callahan et al . , 1976; Kettman et al., 1976), or in
normal cell DNA from BLV-infected cows (Kettmann et al . ,
1978a) .

The BLV provirus is integrated in several sites of
the lymphocyte DNA in cattle with persistent lymphocytosis,
but in only one or a few sites in the DNA of cells of
lymph node tumors (Kettmann et al . , 1979a, 1980a, 1980b).
Less than 5% of peripheral lymphocytes in asymptomatic,
infected cattle contain the provirus, whereas up to 33% of



the circulating lymphocytes in cattle with persistent
lymphocytosis contain the provirus (Kettmann et al . , 1930b).

Seroconversion Period

Seroconversion following infection with BLV has been
found to occur between two and seven weeks in cattle ex-
perimentally inoculated (Mammerickx et al., 1980; Van Der
Maaten and Miller, 1978a, 1978b) . Half of the animals in
these studies had seroconverted by five weeks postinocula-
tion. The seroconversion period was similar for sheep
experimentally inoculated by the intradermal route, oral
route, or by BLV-carrying tabanid flies (Gentile and Rutili,
1978; Mammerickx et al . , 1980; Ohshima et al . , 1981). The
seroconversion period for animals naturally infected is
considered to be less than three months (Straub, 1978b) ,
and the pattern of seroconversion is believed to be similar
to that for experimentally infected animals (Van Der Maaten
and Miller, 1978b) .

Transmission Via Excretions and Secretions

It is well documented that BLV can be experimentally
transmitted to cattle via blood (Mammerickx et al . , 1980;
Van Der Maaten et al . , 1981a) and lymphocytes (Miller and
Van Der Maaten, 1978b; Van Der Maaten and Miller, 1978a,
1978b) from infected animals. The virus has been demon-
strated in saliva but not in prostatic fluid or feces of
infected cattle (Ressang et al . , 1980). The p-24 antigen



of BLV has been found 'in urine of naturally infected
animals (Gupta and Ferrer, 1980) .

Semen collected by manual massage from a BLV-infected
bull transmitted BLV infection to susceptible sheep (Lucas
et al., 1980). Another study failed to demonstrate BLV in
semen collected from BLV-infected bulls following normal
ejaculation (Miller and Van Der Maaten, 1979) .

Serology

Several serologic tests for the detection of BLV have
been described for both the gp-51 and the p-24 antigen

(Burny et al . , 1980). Agar-gel immunodiffusion using gp-51
has been recommended for use by member countries of the
European Economic Community (Kaaden and Stephenson, 1978),
because of its high sensitivity, simplicity, and low cost

(Miller, 1980). Recently a radioimmunoassay procedure
was described using gp-51 (Bex et al., 1979). This test
may be the most sensitive one presently available (Miller
et al. , 1981) .

Factors Examined for Associations with Bovine
Leukemia Virus Infection

Genetic Susceptibility

A genetic predisposition to enzootic bovine leukosis
and bovine lymphosarcoma was suspected before discovery of
BLV. Leukosis was observed more frequently in daughters
of affected cows than in daughters of unaffected cows



10

(Bendixen, 1965; Larson et al . , 1970). Pedigree studies of
lymphosarcoma found clustering of cases by sire and/or dam
families (Crowshaw et al . , 1963; Cypess et al . , 1974;
Marshak et al., 1962). It also was observed that herds
which v/ere inbred experienced higher rates of leukosis and
lymphosarcoma than did noninbred herds (Abt, 1968; Laktionov
and Nakhmanson, 1972) , but purebred herds were found to
have lower rates of leukosis than nonpurebred herds
(Anderson et al . , 1971).

One study estimated the heritability of susceptibility
to BLV infection to be 0.44 ±0.22 (Burridge et al . , 1979).
A study of lymphosarcoma, however, was not able to associate
the disease with serologically defined antigens controlled
by the BoLA-A locus (Takashima and Olson, 1978) .

Parental Infection with Bovine Leukemia Virus

The effect of BLV infection of the dam on subsequent
BLV infection in the offspring has been examined by several
investigators. In one report, dam status appeared to have
a significant influence on progeny infection (Baumgartener
et al . , 1978), but the authors felt that such an effect may
have been due to high prevalence rates in som.e herds. In a
longitudinal study, no association was found between dam
status and age at which progeny became infected (Olson et
al., 1978). Reports on cross-sectional studies concluded
that presence of BLV antibodies in the dam was not associ-
ated with subsequent progeny infection (Hofirek, 1980;
Valikhov, 1973) .



11

In a large study of progeny from BLV-infected, AI bulls,
offspring from infected sires did not have as high a rate of
subsequent BLV infection as did those from noninfected sires
(Baumgartener et al., 1978).

Sex

Few studies have examined for associations between
BLV infection and sex. Reports in which sex effects were
studied suggested no difference in infection rates between
males and females (Baumgartener et al . , 1975; Evermann et
al., 1980) .

Breed

It has been reported that many different breeds are
susceptible to BLV infection (Burridge et al . , 1981; Marin
et al., 1978). Analysis of data from a survey of Florida
cattle suggested that Jerseys had a higher infection rate
than Holsteins (Burridge et al . , 1981). However, a study
within a Florida dairy herd indicated no difference existed
between rates of infections for Jerseys and Holsteins
(Burridge et al., 1979).

Age

Age-specific prevalence rates of BLV infection have
been shown to follow a characteristic sigmoidal curve.
Rates increased linearly from one to four years of age,
after which they plateaued (Burridge et al . , 1979, 1981;



12

Chander et al,, 1978; Evermann et al . , 1980; Ferrer et al . ,
1976; Hofirek, 1980; Mammerickx et al . , 1978a, 1978b;
Marin et al . , 1978; Olson et al . , 1973; Piper et al . , 1979).
Peak prevalence rates of infection were observed at four
years of age in beef cattle and at more than nine years of
age in dairy cattle (Burridge et al., 1981). Ages at which
a sharp, linear increase in rates occurred varied from study
to study and from herd to herd. In some herds rates of
infection began to level off at two to four years of age
(Burridge et al . , 1979; Olson et al . , 1973), while in other
herds rates reached a plateau at four to five years of age
(Chander et al . , 1978; Hofirek, 1980; Mammerickx et al . ,
1978a, 1978b; Marin et al . , 1978).

A few studies have approached age-specific rates of
infection in a longitudinal design using birth cohorts..
Results of one of these investigations showed that animals
of similar ages experienced different rates of infection,
according to the birth cohort (Wilesmith et al . , 1980).
In the other study, each new 12-month cohort entered the
herd with a lower prevalence rate than did the previous
cohort. Rates within a cohort did not appear to change as
cattle aged. It was suggested further that higher preval-
ence rates of infection observed in older animals in
cross-sectional studies represented high-rate cohorts
(Ruber et al . , 1981) .



13



Transmission of Bovine Leukemia Virus Infection

In Utero

Rates of natural in utero infection with BLV have been
reported to range from 3% to 25% (Ferrer et al., 1976,
1977a, 1977b; Piper et al . , 1979). Stage of gestation dur-
ing which a dam is experimentally infected has not been
associated with the frequency of infection in progeny (Van
Der Maaten et al . , 1981b).

Physical Contact

Close physical contact between infected and susceptible
cattle is believed to be a prerequisite to BLV transmission
(Ferrer and Piper, 1981; Maas-Inderwiesen et al . , 1978;
Miller and Van Der Maaten, 1978a; Wilesmith et al . , 1980).
Newborn calves were more likely to develop leukosis when
placed in close contact with leukotic cows (Straub, 1971) .
Infection rates increased during winter months in one herd
studied, suggesting transmission associated with indoor
housing conditions (VJilesmith et al., 1980). Limiting
physical contact by vacating a stall between animals or by
placing a single fence between animals appeared to retard
transmission of infection (Miller and Van Der Maaten, 1978a).

Arthropod Vectors

Bovine leukemia virus has been isolated from the mid-
gut of horseflies after feeding on a BLV-infected cow



14

(Bech-Nielsen et al . , 1978), In an experimental study,
horsefly transmission of BLV infection to sheep was demon-
strated (Ohshima et al . , 1981), It has been suggested
that high rates of infection observed in animals during
summer months support the hypothesis of vector-borne trans-
mission of BLV infection (Bech-Nielsen et al , , 1978; Onuma
et al . , 1980). Another study, however, observed higher
rates of infection during winter months (VJilesmith et al . ,
1980) .

Ixodes ricinus ticks have been suggested as a possible
explanation for geographic differences in rates of infec-
tion in Sweden (Hugoson and Brattstrom, 1980) ,

Aerosol

Intranasal instillation of BLV-infected lymphocytes
produced infection in one of two calves and an aerosol
exposure to BLV-culture fluids produced infection in two of
two calves (Van Der Maaten and Miller, 1978c) , Both methods,
however, also exposed the oral cavity and the latter method
exposed the conjunctivae.

Oral

Bovine leukemia virus or BLV-like particles have been
identified in milk and colostrum of BLV-infected cows and
cows with lymphosarcoma (Dutcher et al,, 1964; Jensen and
Schidlovsky, 1964; Miller and Van Der Maaten, 1979;
Schulze et al , , 1966), Transmission of BLV by the oral


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