HSV in pancreas, other visceral organs in humans

[Guest guest]

Data from mice and humans is similar. HSV can find its way into a

variety of organs (1-3). If a child is mildly immune suppressed (eg, by

the MMR et al; DE; or by thimerosal; Bernard et al; or by subtle

immune glitches; Warren RP et al), then the child's HSV might find its

way into tissues better served by an absence of HSV. Are we suprised the

Goldberg, Baker, and McCandless report that appx 30% of their ASD

patients respond well to acyclovir?

1. Arch Virol 1994;134(1-2):73-83

Herpes simplex virus type 1 (HSV-1) UL56 gene is involved in viral

intraperitoneal pathogenicity to immunocompetent mice.

Berkowitz C, Moyal M, Rosen-Wolff A, Darai G, Becker Y

A comparison of the pathogenicity in mice of the recombinant herpes

simplex

virus type 1 (HSV-1) strain HSV-1-M-LacZ, in which the UL56 gene has

been

deleted, was made with its parental strain F, following infection in

different

mouse strains. The polymerase chain reaction (PCR) technique was used to

study

the migration of virus DNA in the mouse model. Tissues from adult mice

infected

intraperitoneally (IP) with one of three HSV-1 strains (F, HFEM or

HSV-1-LacZ)

were examined for the presence of viral DNA. DNA of the pathogenic

strain F was

detected in the adrenal glands, spinal cord, brain, liver and pancreas.

DNA of

HSV-1-M-LacZ was detected in the same tissues. However, DNA of the

apathogenic

strain HFEM was detected transiently (on days 2 and 3 p.i., but not days

1, 5 or

7), only in the adrenal glands and no viral DNA was detected in any of

the other

tissues. HSV-1 pathogenic strains injected intraperitoneally into

newborn mice

(7 days old) killed most of the mice. In the surviving mice viral DNA of

the

three virus strains was found in peritoneal exudate cells (PEC), adrenal

glands,

spinal cord, liver and spleen. It was found that HSV-1-M-LacZ, which

lacks the

UL56 gene, resembled in pathogenicity to the newborn mice the pathogenic

HSV-1

strains F and KOS. The PCR technique was used to trace viral DNA in

tissues of

the mice which survived HSV-1 infection at 7 weeks of age. Only HSV-1

(KOS) DNA

was detected in the pancreas. The brains of these mice did not contain

viral

DNA. It is suggested that HSV-1 DNA may reside in surviving HSV-1-

infected

newborn mice in a " latent " state in nonneural tissues.

2. Kansenshogaku Zasshi 1989 Aug;63(8):859-66

[A pathological study on herpes simplex virus infections in adults].

[Article in Japanese]

Tashiro T, Shigeno H, Goto J, Kikuchi H, Terao H, Nasu M

A pathological study was carried out in 200 autopsied cases experienced

in our

department from 1981 to 1988. Eight patients (4.0%) had herpes simplex

virus

(HSV) infections in their visceral organs. Another one patient was

diagnosed as

HSV hepatitis through necropsy of liver. The nine patients (five of them

were

male) ranged in age from 34 to 70 years (mean, 58). Four patients had

non-Hodgkin's lymphoma, and the other included one with adult T-cell

leukemia,

one with multiple myeloma, one with idiopathic interstitial pneumonia

and one

with bronchial asthma, however, one did not have any underlying disease.

Two

patients died of HSV fulminant hepatitis and one died of HSV diffuse

interstitial pneumonia. The most commonly involved organ was esophagus

(7/8),

followed by tongue (5/8), liver (3/9), spleen, pancreas, lymph node

(2/8), and

lung, adrenal, tonsil (1/8). Typical herpetic changes such as ballooning

degeneration of cells, multinucleated giant cells, ground-glass nuclei

and

Cowdry type A intranuclear inclusions were observed at the margin of the

ulcer

or coagulation necrosis. Indirect immunoperoxidase stain revealed HSV-1

antigen

in all of the 9 cases, HSV particles were demonstrated in 2. Seven

patients had

concomitant infections with one or more pathogens in addition to HSV,

which

included cytomegalovirus in 5, aspergillus in 4, candida in 3 and

bacteria in 3.

3. Transplantation 1989 Apr;47(4):609-13

Possible transmission of herpes simplex virus by organ transplantation.

Goodman JL

Department of Medicine, Minnesota Hospital and Clinics School of

Medicine,

Minneapolis 55455.

Herpes simplex virus commonly reactivates in seropositive transplant

recipients

but has not been generally thought to be transmissible by the

transplanted organ

itself. We studied two consecutive cases of disseminated HSV, without

mucosal

lesions, occurring in a heart and in a pancreatic transplant recipient,

and

implicate the allografts as the source of the virus. In both cases the

recipients were seronegative pretransplant by complement fixation (less

than

1:4), neutralization (less than 1:2), and complement enhanced

neutralization

(less than 1:4), and by radioimmunoprecipitation of HSV-2 antigens with

serum

followed by polyacrylamide gel electrophoresis (RIPA-PAGE). Both

recipients'

isolates were HSV-2 by restriction mapping and each donor had antibodies

directed specifically against HSV-2, as determined by differential

neutralization (HSV-2/HSV-1 ratios 1.46 and 1.58, where greater than

0.85

indicates antibody to HSV-2). Posttransplant, each recipient developed

an

antibody response with temporal antigenic specificity and

complement-enhanced

neutralization consistent with primary infection. These findings have

important

clinical and pathogenic implications and suggest that latent or

reactivated

HSV-2 DNA transplanted in donor tissues may cause severe infection in

seronegative and immunosuppressed transplant recipients.