Yoshiya Ando

Primary infection of Japanese infants with adult T-cell leukaemia-associated retrovirus (ATLV): Evidence for viral transmission from mothers to children

Primary infection with adult T-cell leukemia virus (ATLV) was investigated by follow-up studies on 16 ATLV-seropositive mothers and their breastfed infants in an ATLV-endemic area of Japan. Maternal antibody to ATLV decreased in all the infants, and was detectable in only three of 12 infants tested 6 months after birth. Reappearance of the antibody 9-18 months after birth was observed in only four of the 16 infants. The ATLV-bearing cells in peripheral blood were detected in all 16 mothers after delivery. None of the 16 infants showed ATLV-bearing cells in peripheral or cord blood sampled at birth, or 1, 3 or 6 months after birth. However, virus-bearing cells in the blood became detectable 9-18 months after birth in 13 of the 16 infants. Maternal antibody and virus-bearing cells were never detected in a control group of seven infants of ATLV-seronegative mothers. These findings provide evidence for the high incidence of primary ATLV infection during early infancy among infants born to ATLV-seropositive mothers and suggest maternal viral transmission. Furthermore, samples of breast milk from all 12 seropositive mothers examined contained cell-associated ATLV capable of being transmitted to peripheral leucocytes of neonates. This finding suggests that one of the possible maternal transmission routes of ATLV is via breast milk.

Bottle-feeding can prevent transmission of htlv-1 from mothers to their babies

Breast-feeding is a major factor in the vertical transmission of human T-lymphotropic virus type I (HTLV-I). We studied whether such transmission may be prevented by bottle-feeding. HTLV-I infection was detected by both HTLV-I antigen and antibody tests. Thirty bottle-fed babies were examined 24 months after birth; only one was found to be HTLV-I antigen-positive. This infection rate was lower than that for breast-fed babies in whom HTLV-I antigen was detected in 24 of the 31 24-month-old babies born to HTLV-I positive mothers in a previous study. These results suggest that most vertical transmission of HTLV-I is attributable to breast-feeding and can be prevented by bottle-feeding.

Identification of HTLV‐I Sequence in Cord Blood Mononuclear Cells of Neonates Born to HTLV‐I Antigen/Antibody‐positive Mothers by Polymerase Chain Reaction

We developed a polymerase chain reaction (PCR) method which has high sensitivity and simple technique in order to investigate the presence or absence of human T lymphotropic virus type I (HTLV‐I) provirus in cord blood mononuclear cells of neonates born to HTLV‐I carrier mothers. Out of 40, three subjects were found to contain the HTLV‐I provirus genome. These three subjects remained HTLV‐I sequence‐positive in follow‐up study. On the other hand, when examined by a conventional technique for detection of HTLV‐I‐associated antigen on peripheral mononuclear cells, all 40 neonates were HTLV‐I‐associated antigen‐negative. These results suggest that PCR is more sensitive than the conventional antigen detection method and is useful in early detection of HTLV‐I infection in neonates born to HTLV‐I carriers.

HHV-6 infection during pregnancy and spontaneous abortion

antibody titres of her serum, because serum antibody titres for viruses that induce liver dysfunction generally were negative. HHV-6 antibody rose from under 10 at admission to over 1280 after 4 days, and high titres were maintained for 3 months (> 1280) (figure). We suspected that her symptoms were caused by chronic HHV-6 infection and began daily intravenous injection of stronger neominophagen C (SNMC) containing glycyrrhizon and subcutaneous injections of recombinant G-CSF 25 ug (GRAN, Sankyo). SNMC therapy was ineffective. Her liver dysfunction worsened and granulocytopenia (segmentation 0%, band 0%) and anaemia (Hb 7-8 g/dl) continued. In May, she had mild jaundice (total bilirubin 1 4 mg/dl) and in June her aminotransferase values were increased (ALT 1949 and AST 1155 IU/1). To reduce virus activity, we administered interferon-ot (IFN-(x, Sumitomo) by daily subcutaneous injection, similar to the protocol for chronic hepatitis caused by hepatitis B or C viruses. We started at 20 000 U/kg per day and increased to 80 000 U/kg per day. Liver dysfunction improved (ALT 517 and AST 393 IU/1) 1 month later, and granulocytopenia and anaemia improved slowly. There have been no reports of progressive liver dysfunction, anaemia, and granulocytopenia associated with HHV-6 infection. All the symptoms in our case were suspected to have been caused by HHV-6 chronic active infection because of the clinical symptoms and the changes in HHV-6 antibody titre.

Detection of HTLV-I Genome in Seronegative Infants Born to HTLV-I Seropositive Mothers by Polymerase Chain Reaction

We applied the polymerase chain reaction (PCR) method to detect gag, env and pX sequences of human T cell leukemia virus type I (HTLV‐I) provirus in peripheral blood lymphocytes of seronega‐tive infants born to HTLV‐I seropositive mothers. Out of 22, five subjects were found to contain the HTLV‐I provirus genome. Two of the five cases were judged to be negative for not only anti‐HTLV‐I antibodies but also the viral antigens on cultivated lymphocytes by the conventional antibody/antigen detection methods. These results indicate that PCR is of great use as a simple and highly sensitive method detect HTLV‐I infection.

Family study of women showing development of antibody to human T-cell leukemia virus I and assessment of the risk of vertical transmission of the virus to their children

When pregnant women were tested for antibody to human T-cell leukemia virus-I, some were found to be positive although they had been negative during the previous pregnancy. In these women, HTLV-I infection was found from pedigree studies to have been acquired from their mothers rather than from their husbands. Furthermore, some of them had apparently remained HTLV-I antibody-negative for long periods after infection. When the breast-fed children of these women, in whom HTLV-I was acquired from their mothers but who were in an HTLV-I antibody-negative state, were also examined for evidence of HTLV-I infection, none was found.