The protective effects of passively administered antibodies against hantavirus infection were studied in newborn rats. Death as well as infection were completely prevented from intraperitoneal challenge of strain SR-11 (SR) (2 x 10(3) FFU, 10(2.1) LD50), in newborn rats which received 0.1 ml of anti-SR rat serum (neutralizing antibody titer, 1:640) 4 hr before the virus challenge. In these rats, no virus was detected in the peritoneal macrophages, lung, kidney, and brain. The immune serum infusion before the virus challenge also conferred protection to rats against an intramuscular or subcutaneous challenge of strain SR, but did not protect the rats against intracerebral challenge of the virus. In the rats which received the immune serum after the challenge, infection was not prevented, although some of the animals were protected from the death. Virus titers in the lung, kidney, and brain of the rats were reduced by the transfer of the immune serum even as late as 72 hr after the challenge. Cross-protection in the rats which received the immune serum was strong between strains SR and KI-262 within the same serotype, but very weak between strains SR and Hantaan 76-118 of different serotypes.
Two strains of hemorrhagic fever with renal syndrome (HFRS) virus from Rattus, SR-11 and KI-262, showed virtually identical antigenicity but differed from prototype strain Hantaan 76-118 (Apodemus origin) in a neutralization test. Wistar newborn rats inoculated intraperitoneally (i.p.) with SR-11, which was isolated from a laboratory rat associated with an outbreak of HFRS, developed clinical signs such as ataxia and limb paralysis and died at about 18 days after inoculation. The LD50 of SR-11 in 1-day-old rats was 101.2 focus-forming units (FFU). In contrast, the animals inoculated i.p. or intracerebrally with 104 FFU of KI-262, which was from a wild rat in a dumping-ground area-an enzootic focus where no human cases have been recorded-did not show any significant clinical signs. The susceptibility of rats to SR-11 fatal infection was age-dependent. Virus titers in brains, lungs, kidneys, and livers of the rats inoculated with SR-11 were significantly higher than those in the same organs of the animals infected with KI-262. Necrosis of neurons in the brain tissue occurred in the rats infected with SR-11, while it was mild in the animals infected with KI-262.
Eight cell lines were established from patients with adult T‐cell leukemia, and from normal adults, by cocultivation with human T‐cell leukemia virus type I(HTLV‐I)‐producer cell lines in the presence of interleukin‐2. All of these cell lines harbored HTLV‐I and showed T‐cell markers CD2, CD3 and CD4, hut not B‐cell markers. Unexpectedly, all eight cell lines expressed a myeloid marker CD13 and three of the eight lines also expressed another myeloid marker CD33. Dual staining showed the simultaneous expression of CD3 and CD13 on the same cells. Thus, evidence was obtained for the expression of myeloid antigens on HTLV‐I‐harboring T cells.
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