Sclerosing Panencephalitis During Pregnancy
Subacute A
Surviving Normal Infant
Kenneth J. Gaines, MD; J. T. Jabbour, MD; John N. Whitaker, MD; John Sever, MD, PhD
\s=b\ A
normal infant
was
born to a 15subacute the fifth
year-old girl who developed sclerosing panencephalitis in
month of pregnancy. The serum measles antibody titers of the infant gradually declined during the first year of life. The child, now age 3, has no neurological abnormalities. (Arch Neurol 36:314-316, 1979)
Although the relationship of rubeola subacute sclerosing panenceph¬
*"* to
alitis (SSPE) has been well estab¬ lished, the pathogenetic mechanisms
remain poorly defined and under¬ stood. The appearance of SSPE in unusual situations, ie, in siblings14 or in only one of identical twins,5·6 permits an analysis of possible patho¬ genetic factors. This report describes the occurrence of SSPE in a pregnant girl and the results of studies per¬ formed on the infant. Accepted
for publication July 25, 1978. From the Department of Neurology, University of Tennessee Center for the Health Sciences, Memphis (Drs Gaines and Whitaker); the Department of Pediatric Neurology, LeBonheur Children's Hospital, Memphis (Dr Jabbour); the Neurology Service, Memphis Veterans Hospital (Dr Whitaker); and the Infectious Disease Section, National Institute of Neurology and Communicative Disorders and Stroke, Bethesda, Md. Reprint requests to Department of Pediatric Neurology, LeBonheur Children's Hospital, 848 Adams Ave, Memphis, TN 38103 (Dr Jabbour).
REPORT OF A CASE A 15-year-old girl was well until Decem¬ ber 1973, during her first pregnancy, when she experienced vague pain in her neck and numbness of her hands. Changes in person¬ ality were noted. She was treated with thioridazine, but three days later became withdrawn and complained that she was blind. In January 1974, she was regarded as schizophrenic. Two weeks later, stiffness of the neck with deviation of the head to the left, intermittent jerking of the extremities, and weakness of the left arm led to hospital admission on Jan 28, 1974. She had had measles at age 2 and mumps, varicella, and herpes zoster be¬ tween ages 12 and 13. The vital signs were normal. She lay quietly with eyes open and appeared to be awake. She responded to her name but not to other verbal stimuli. She responded to painful stimuli in all extremities by with¬ drawal and crying. Funduscopic findings were normal. The eyes were conjugately deviated to the left, but would move conju¬ gately to the right with the oculocephalic maneuver. The head, continuously deviated to the left, resisted any movement. Myoclo¬ nus was noted in the right arm and left leg. Muscle stretch reflexes were brisk and symmetrical, with an extensor plantar response on the right. There was an intra¬ uterine pregnancy in advanced gestation, with the cervix closed, and no evident fetal distress. Except for herpetic-like lesions of the lips, the rest of the findings were unremarkable. Cerebrospinal fluid studies on Jan 13, 1974, demonstrated four mononuclear cells, eight erythrocytes, glucose concentration of 74 mg/dL, and protein concentration of
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/10/2015
55 mg/dL. The CSF -globulin level was 62%. The CSF rubeola antibody titer was 1:32 (Table). Two EEGs showed an irregular slow background with periodic bursts of highvoltage slow waves (Fig 1). Urinalysis, blood cell count, and electrolyte, BUN, and glucose values were normal. Liver function tests were abnormal, with an SGOT level of 90 IU/L and a serum alkaline phosphatase level of 134 kA units/dL, and remained so throughout the hospitalization; no cause was determined and liver biopsy was not thought advisable. Labor was induced and a 3,180-g infant was delivered uneventfully. The Apgar score was 10 and the child showed no neurologic or other abnormalities. A CSF sample of the infant taken two days after birth demonstrated no cells, normal glucose and protein concentrations, and a rubeola titer of 1:4. The rubeola titer on the cord blood was 1:128, and the infant's serum rubeola titer was 1:64 at birth (Table).
RESULTS
Clinical and laboratory evaluations of the child and mother have been performed at intervals over three years. The child has developed normal¬ ly and has shown no abnormalities on neurological or EEG examination. The mother's condition has continued to worsen, with mental deterioration and increased spasticity but disappear¬ ance of the myoclonus (Fig 2). She is now uncommunicative and requires complete care. Laboratory studies dis¬ closed a gradual disappearance of rubeola antibodies in the CSF and
Serologie Measles
Serum CSF Serum CSF
6/75 Cord blood 2/26/74 Infant 2/28/74
Hemagglutinin
Fixation
Inhibition
1:256
1:128 1:32
1:32 ND* ND
Serum CSF Serum CSF
2/15/75
not received measles
Antibody Titer
Complement Mother 1/74
of the infant. The infant has vaccine, but other vaccines have been given. serum
Data
CSF
COMMENT
-globulin, %
This report describes a mother with SSPE during pregnancy who was delivered of a normal infant who is surviving and well. Criteria for the diagnosis of SSPE in the mother were adequate. The infant, at 3 years of age, has not yet manifested any
62
ND
ND
ND
1:128
1:64 1:4 1:54 ND
1:64
53.9
neurologic abnormality.
F8-A2
W
KL
^.
ri
W.\^'
Fig 1 .—Electroencephalogram
of mother. J refers to
1973
Conception
myoclonic jerks.
t
t July
February
December 1973 Clinical Onset of SSPE
Fig 2—Clinical
May
1974
1975
Delivery
Follow-up
a* 8 Months'
Gestation course
case
reported
1:4 ND
"Not done.
· !
of SSPE has been previously in a 21-year-old woman who was pregnant at onset of symptoms.7 She was delivered after 34 weeks' ges¬ tation of a 2.3-kg infant who died 24 hours later of respiratory distress syn¬ drome, severe anemia, and subdural hematoma. The infant's brain showed no histologie evidence of encephalitis. Serologie data were not reported. There is an abundant documenta¬ tion that measles-like virus is the etiologic agent in SSPE, which although not identical to, shares many charac¬ teristics with, wild and vaccine strains of rubeola virus.8 Rubeola virus can cross the placental barrier as can a number of other viruses.9 Transplacental transmission of the virus is possible at any stage of gestation and has been demonstrated at time of abortion in stillbirth and at live births. In the majority of pregnancies compli¬ cated by rubeola, there are no abnor¬ malities in the fetus.1"14 The SSPE agent differs from conventional mea¬ sles virus in its affinity for cells in tissue culture.5 The virus has not been cultured from blood and the elevated antibody level in blood would make the presence of viable free virus most unlikely. Presumably, there was no viremia to produce infection of the fetus in the present case. The immunological studies do not support active infection in this infant. Rubeola antibody readily traverses the placental barrier. Infants having passively received antibody from the mother showT serum levels equal to the mother at birth and a gradual decline in the level over four months. After six months, any antibody present is produced by the infant.11 In this case, the infant's rubeola antibody titer fell in a pattern expected with antibody derived from a maternal source.14 The normal serum-CSF ratio for viral antibodies ranges from 160:1 to 1T 2,000:1, with a mean of 500:1.' In SSPE, the serum-CSF ratio for rubeo¬ la antibody is altered and ranges from 2:1 to 64:118"'9; this may be evidence of local production of antibody within the CNS.17 In this case, the ratio of 4:1 A
1:4
of mother.
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/10/2015
in the mother is consistent with SSPE. The ratio was 16:1 in the infant, and raises the question whether this
represented antibody passively trans¬ mitted across a poorly developed blood-brain barrier or antibody locally produced in the CSF of the fetus. A study by Thorley et al·'" evaluated serum and CSF antibody titers of
newborn infants born to mothers who had had prior exposure to diphtheria and tetanus and who had evaluated antibody viral titers. The hemagglutinin inhibition titers were higher in the serum than in the CSF, and the mean serum-CSF ratio was 14:1 for diphtheria and 26:1 for tetanus. They concluded that this was a typical ratio for passively transmitted antibody into the newborn CSF. The ratio of 16:1 in this infant falls within a simi-
lar range and suggests passively transmitted antibody. Rubeola, teta¬ nus, and diphtheria antibodies pass the placenta readily. The data and course failed to show evidence of infection by the SSPE agent in the infant, although presum¬ ably there was a potential for infec¬ tion throughout the entire gestation. Also, the infant had rubeola antibody to the SSPE agent in blood and in CSF for at least the period directly preced¬ ing and following birth. Its presence there was not sufficient to produce the disease and hence calls into ques¬ tion a primary role for the antibody alone in SSPE. A peculiar host suscep¬ tibility or stage of maturity may be
important.
The SSPE agent could have infected the infant, failed to induce an immu-
nologic response, but remained viable in an immunologically tolerant host. It has been postulated that tolerance
between virus and host immune mech¬ anism allows for persistent cell infec¬ tion with SSPE agent."1 Such an infec¬ tion can be induced in the hamster.--' Newborn hamsters inoculated with rubeola virus intracerebrally develop encephalitis, but animals protected by high levels of maternal rubeola anti¬ body develop persistent intracellular virus and do not develop encephalitis for 30 to 60 days. A similar phenome¬ non has been reported-1 following in vivo infection of mice with lymphocyt¬ ic choriomeningitis virus; in these animals, the tolerant state persists for 10 to .2 months before onset of symp¬ toms.
References 1. Chien
LT, Wilborn WH, Casey J,
simultaneous
et al: The
sclerosing panencepahlitis Clinical, virologic, and histopathologic studies. J Infect Dis occurrence
of subacute
in two brothers: I.
125:123-128, 1975.
2. Lorland B, Nogy T, Tariska S: Subacute sclerosing panencephalitis. World Neurol 3:376394, 1962. 3. Clark NS, Best PV: Subacute sclerosing (inclusion body) encephalitis. Arch Dis Child
39:356-362, 1964. 4.
Kennedy C: A ten-year experience with sclerosing panencephalitis. Neurology
subacute
18:58-59, 1968.
5. D'Anghia C, Lefevre AB, Carelas HM et al: Subacute sclerosing panencephalitis in only one member of a monozygotic twin pair. J Neurol Sci 21:323-332, 1974. 6. Whitaker J, Sever JL, Engel W: Subacute sclerosing panencephalitis in only one of identical twins. N Engl J Med 287:864-866, 1972. 7. Nelson RF, Dennesy JM: SSPE and pregnancy. Lancet 1:1289, 1972. 8. Ter Meuler V, Katz M, Muller D: Subacute
sclerosing panencephalitis: A review. Curr Top Microbiol Immunol 57:1-38, 1972. 9. Monif GRC: Infectious Diseases in Obstetrics and Gynecology. New York, Harper & Row Publishers, 1974, p 33. 10. Dyer I: Measles complicating pregnancy. South Med J 33:601-604, 1940. 11. Parker AO: The influence of maternal measles (morbilli) on the unborn child. Med J Aust 1:835-837, 1950. 12. Swan C, Tosterin AL, Basham-Black GH: Final observation on congenital defects in infants following infectious diseases during pregnancy. Med J Aust 2:889-908, 1946. 13. Currie GA: Immunology of pregnancy: The foetal maternal barrier. Proc R Soc Med 61:1206, 1968. 14. Overall JC, Glasgow LA: Virus infections of the fetus and newborn. J Pediatr 77:315-333, 1970. 15. Adams JM, Imagaus DJ: Measles antibodies in multiple sclerosis. Proc Soc Exp Biol Med 3:562-566, 1962. 16. Clarke JK, Dane DS, Dick GWA: Viral
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/10/2015
in the CSF and serum of multiple sclerosis patients. Brain 88:953-962, 1965. 17. Link H, Pandius M, Salini AA: Immunoglobulins and measles antibody and antigen in subacute sclerosing panencephalitis. Arch Neurol 28:23-28, 1973. 18. Connolly JH, Allen IV, Hurwitz LJ, et al: Measles virus antibody and antigen in subacute sclerosing panencephalitis. Lancet 1:542, 1967. 19. Johnson RT: Slow infections of the nervous system and the subacute spongiform encephalopathics. Adv Neurol 6:69-75, 1974. 20. Thorley JD, Holmes RK, Kaplan JM, et al: Passive transfer of antibodies of maternal origin from blood to CSF in infants. Lancet 1:651-653, 1975. 21. Brody J, Detels R: Subacute sclerosing panencephalitis: A zoonosis following aberrant measles. Lancet 2:500, 1970. 22. Wear D, Rapp F: Latent measles virus infection of the hamster central nervous system. J Immunol 107:1593, 1971. 23. Hotchkin J: Persistent and slow virus infections. Monogr Virol 3:2-60, 1974.
antibody
Subacute A
Surviving Normal Infant
Kenneth J. Gaines, MD; J. T. Jabbour, MD; John N. Whitaker, MD; John Sever, MD, PhD
\s=b\ A
normal infant
was
born to a 15subacute the fifth
year-old girl who developed sclerosing panencephalitis in
month of pregnancy. The serum measles antibody titers of the infant gradually declined during the first year of life. The child, now age 3, has no neurological abnormalities. (Arch Neurol 36:314-316, 1979)
Although the relationship of rubeola subacute sclerosing panenceph¬
*"* to
alitis (SSPE) has been well estab¬ lished, the pathogenetic mechanisms
remain poorly defined and under¬ stood. The appearance of SSPE in unusual situations, ie, in siblings14 or in only one of identical twins,5·6 permits an analysis of possible patho¬ genetic factors. This report describes the occurrence of SSPE in a pregnant girl and the results of studies per¬ formed on the infant. Accepted
for publication July 25, 1978. From the Department of Neurology, University of Tennessee Center for the Health Sciences, Memphis (Drs Gaines and Whitaker); the Department of Pediatric Neurology, LeBonheur Children's Hospital, Memphis (Dr Jabbour); the Neurology Service, Memphis Veterans Hospital (Dr Whitaker); and the Infectious Disease Section, National Institute of Neurology and Communicative Disorders and Stroke, Bethesda, Md. Reprint requests to Department of Pediatric Neurology, LeBonheur Children's Hospital, 848 Adams Ave, Memphis, TN 38103 (Dr Jabbour).
REPORT OF A CASE A 15-year-old girl was well until Decem¬ ber 1973, during her first pregnancy, when she experienced vague pain in her neck and numbness of her hands. Changes in person¬ ality were noted. She was treated with thioridazine, but three days later became withdrawn and complained that she was blind. In January 1974, she was regarded as schizophrenic. Two weeks later, stiffness of the neck with deviation of the head to the left, intermittent jerking of the extremities, and weakness of the left arm led to hospital admission on Jan 28, 1974. She had had measles at age 2 and mumps, varicella, and herpes zoster be¬ tween ages 12 and 13. The vital signs were normal. She lay quietly with eyes open and appeared to be awake. She responded to her name but not to other verbal stimuli. She responded to painful stimuli in all extremities by with¬ drawal and crying. Funduscopic findings were normal. The eyes were conjugately deviated to the left, but would move conju¬ gately to the right with the oculocephalic maneuver. The head, continuously deviated to the left, resisted any movement. Myoclo¬ nus was noted in the right arm and left leg. Muscle stretch reflexes were brisk and symmetrical, with an extensor plantar response on the right. There was an intra¬ uterine pregnancy in advanced gestation, with the cervix closed, and no evident fetal distress. Except for herpetic-like lesions of the lips, the rest of the findings were unremarkable. Cerebrospinal fluid studies on Jan 13, 1974, demonstrated four mononuclear cells, eight erythrocytes, glucose concentration of 74 mg/dL, and protein concentration of
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/10/2015
55 mg/dL. The CSF -globulin level was 62%. The CSF rubeola antibody titer was 1:32 (Table). Two EEGs showed an irregular slow background with periodic bursts of highvoltage slow waves (Fig 1). Urinalysis, blood cell count, and electrolyte, BUN, and glucose values were normal. Liver function tests were abnormal, with an SGOT level of 90 IU/L and a serum alkaline phosphatase level of 134 kA units/dL, and remained so throughout the hospitalization; no cause was determined and liver biopsy was not thought advisable. Labor was induced and a 3,180-g infant was delivered uneventfully. The Apgar score was 10 and the child showed no neurologic or other abnormalities. A CSF sample of the infant taken two days after birth demonstrated no cells, normal glucose and protein concentrations, and a rubeola titer of 1:4. The rubeola titer on the cord blood was 1:128, and the infant's serum rubeola titer was 1:64 at birth (Table).
RESULTS
Clinical and laboratory evaluations of the child and mother have been performed at intervals over three years. The child has developed normal¬ ly and has shown no abnormalities on neurological or EEG examination. The mother's condition has continued to worsen, with mental deterioration and increased spasticity but disappear¬ ance of the myoclonus (Fig 2). She is now uncommunicative and requires complete care. Laboratory studies dis¬ closed a gradual disappearance of rubeola antibodies in the CSF and
Serologie Measles
Serum CSF Serum CSF
6/75 Cord blood 2/26/74 Infant 2/28/74
Hemagglutinin
Fixation
Inhibition
1:256
1:128 1:32
1:32 ND* ND
Serum CSF Serum CSF
2/15/75
not received measles
Antibody Titer
Complement Mother 1/74
of the infant. The infant has vaccine, but other vaccines have been given. serum
Data
CSF
COMMENT
-globulin, %
This report describes a mother with SSPE during pregnancy who was delivered of a normal infant who is surviving and well. Criteria for the diagnosis of SSPE in the mother were adequate. The infant, at 3 years of age, has not yet manifested any
62
ND
ND
ND
1:128
1:64 1:4 1:54 ND
1:64
53.9
neurologic abnormality.
F8-A2
W
KL
^.
ri
W.\^'
Fig 1 .—Electroencephalogram
of mother. J refers to
1973
Conception
myoclonic jerks.
t
t July
February
December 1973 Clinical Onset of SSPE
Fig 2—Clinical
May
1974
1975
Delivery
Follow-up
a* 8 Months'
Gestation course
case
reported
1:4 ND
"Not done.
· !
of SSPE has been previously in a 21-year-old woman who was pregnant at onset of symptoms.7 She was delivered after 34 weeks' ges¬ tation of a 2.3-kg infant who died 24 hours later of respiratory distress syn¬ drome, severe anemia, and subdural hematoma. The infant's brain showed no histologie evidence of encephalitis. Serologie data were not reported. There is an abundant documenta¬ tion that measles-like virus is the etiologic agent in SSPE, which although not identical to, shares many charac¬ teristics with, wild and vaccine strains of rubeola virus.8 Rubeola virus can cross the placental barrier as can a number of other viruses.9 Transplacental transmission of the virus is possible at any stage of gestation and has been demonstrated at time of abortion in stillbirth and at live births. In the majority of pregnancies compli¬ cated by rubeola, there are no abnor¬ malities in the fetus.1"14 The SSPE agent differs from conventional mea¬ sles virus in its affinity for cells in tissue culture.5 The virus has not been cultured from blood and the elevated antibody level in blood would make the presence of viable free virus most unlikely. Presumably, there was no viremia to produce infection of the fetus in the present case. The immunological studies do not support active infection in this infant. Rubeola antibody readily traverses the placental barrier. Infants having passively received antibody from the mother showT serum levels equal to the mother at birth and a gradual decline in the level over four months. After six months, any antibody present is produced by the infant.11 In this case, the infant's rubeola antibody titer fell in a pattern expected with antibody derived from a maternal source.14 The normal serum-CSF ratio for viral antibodies ranges from 160:1 to 1T 2,000:1, with a mean of 500:1.' In SSPE, the serum-CSF ratio for rubeo¬ la antibody is altered and ranges from 2:1 to 64:118"'9; this may be evidence of local production of antibody within the CNS.17 In this case, the ratio of 4:1 A
1:4
of mother.
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/10/2015
in the mother is consistent with SSPE. The ratio was 16:1 in the infant, and raises the question whether this
represented antibody passively trans¬ mitted across a poorly developed blood-brain barrier or antibody locally produced in the CSF of the fetus. A study by Thorley et al·'" evaluated serum and CSF antibody titers of
newborn infants born to mothers who had had prior exposure to diphtheria and tetanus and who had evaluated antibody viral titers. The hemagglutinin inhibition titers were higher in the serum than in the CSF, and the mean serum-CSF ratio was 14:1 for diphtheria and 26:1 for tetanus. They concluded that this was a typical ratio for passively transmitted antibody into the newborn CSF. The ratio of 16:1 in this infant falls within a simi-
lar range and suggests passively transmitted antibody. Rubeola, teta¬ nus, and diphtheria antibodies pass the placenta readily. The data and course failed to show evidence of infection by the SSPE agent in the infant, although presum¬ ably there was a potential for infec¬ tion throughout the entire gestation. Also, the infant had rubeola antibody to the SSPE agent in blood and in CSF for at least the period directly preced¬ ing and following birth. Its presence there was not sufficient to produce the disease and hence calls into ques¬ tion a primary role for the antibody alone in SSPE. A peculiar host suscep¬ tibility or stage of maturity may be
important.
The SSPE agent could have infected the infant, failed to induce an immu-
nologic response, but remained viable in an immunologically tolerant host. It has been postulated that tolerance
between virus and host immune mech¬ anism allows for persistent cell infec¬ tion with SSPE agent."1 Such an infec¬ tion can be induced in the hamster.--' Newborn hamsters inoculated with rubeola virus intracerebrally develop encephalitis, but animals protected by high levels of maternal rubeola anti¬ body develop persistent intracellular virus and do not develop encephalitis for 30 to 60 days. A similar phenome¬ non has been reported-1 following in vivo infection of mice with lymphocyt¬ ic choriomeningitis virus; in these animals, the tolerant state persists for 10 to .2 months before onset of symp¬ toms.
References 1. Chien
LT, Wilborn WH, Casey J,
simultaneous
et al: The
sclerosing panencepahlitis Clinical, virologic, and histopathologic studies. J Infect Dis occurrence
of subacute
in two brothers: I.
125:123-128, 1975.
2. Lorland B, Nogy T, Tariska S: Subacute sclerosing panencephalitis. World Neurol 3:376394, 1962. 3. Clark NS, Best PV: Subacute sclerosing (inclusion body) encephalitis. Arch Dis Child
39:356-362, 1964. 4.
Kennedy C: A ten-year experience with sclerosing panencephalitis. Neurology
subacute
18:58-59, 1968.
5. D'Anghia C, Lefevre AB, Carelas HM et al: Subacute sclerosing panencephalitis in only one member of a monozygotic twin pair. J Neurol Sci 21:323-332, 1974. 6. Whitaker J, Sever JL, Engel W: Subacute sclerosing panencephalitis in only one of identical twins. N Engl J Med 287:864-866, 1972. 7. Nelson RF, Dennesy JM: SSPE and pregnancy. Lancet 1:1289, 1972. 8. Ter Meuler V, Katz M, Muller D: Subacute
sclerosing panencephalitis: A review. Curr Top Microbiol Immunol 57:1-38, 1972. 9. Monif GRC: Infectious Diseases in Obstetrics and Gynecology. New York, Harper & Row Publishers, 1974, p 33. 10. Dyer I: Measles complicating pregnancy. South Med J 33:601-604, 1940. 11. Parker AO: The influence of maternal measles (morbilli) on the unborn child. Med J Aust 1:835-837, 1950. 12. Swan C, Tosterin AL, Basham-Black GH: Final observation on congenital defects in infants following infectious diseases during pregnancy. Med J Aust 2:889-908, 1946. 13. Currie GA: Immunology of pregnancy: The foetal maternal barrier. Proc R Soc Med 61:1206, 1968. 14. Overall JC, Glasgow LA: Virus infections of the fetus and newborn. J Pediatr 77:315-333, 1970. 15. Adams JM, Imagaus DJ: Measles antibodies in multiple sclerosis. Proc Soc Exp Biol Med 3:562-566, 1962. 16. Clarke JK, Dane DS, Dick GWA: Viral
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/10/2015
in the CSF and serum of multiple sclerosis patients. Brain 88:953-962, 1965. 17. Link H, Pandius M, Salini AA: Immunoglobulins and measles antibody and antigen in subacute sclerosing panencephalitis. Arch Neurol 28:23-28, 1973. 18. Connolly JH, Allen IV, Hurwitz LJ, et al: Measles virus antibody and antigen in subacute sclerosing panencephalitis. Lancet 1:542, 1967. 19. Johnson RT: Slow infections of the nervous system and the subacute spongiform encephalopathics. Adv Neurol 6:69-75, 1974. 20. Thorley JD, Holmes RK, Kaplan JM, et al: Passive transfer of antibodies of maternal origin from blood to CSF in infants. Lancet 1:651-653, 1975. 21. Brody J, Detels R: Subacute sclerosing panencephalitis: A zoonosis following aberrant measles. Lancet 2:500, 1970. 22. Wear D, Rapp F: Latent measles virus infection of the hamster central nervous system. J Immunol 107:1593, 1971. 23. Hotchkin J: Persistent and slow virus infections. Monogr Virol 3:2-60, 1974.
antibody
