PARAINFLUENZA Type 1 virus is an important cause of acute respiratory disease in infants and children.^{1 , 2} During primary infection the lower respiratory tract is often involved, and illness may be quite severe. Initial infection usually occurs during childhood, and most older children and adults have serum neutralizing antibody to this virus.² Reinfection with Type 1 virus has been observed in adults under both experimental and natural conditions despite the presence of serum neutralizing antibody.^{3 4 5} Illness associated with reinfection is generally mild and limited to the upper respiratory tract.Adults and older children undergoing reinfection probably constitute an important source of . . .

We report three children with congenital anaemia after intrauterine infection with B19 parvovirus. All the fetuses developed hydrops fetalis that was treated by blood transfusion. After delivery the infants had hypogammaglobulinaemia. In all three, sera lacked B19 but viral DNA was found in bone marrow. All were treated with immunoglobulin. One child died and B19 was found in various tissues. In the other two cases, virus could no longer be detected after therapy but the patients remain persistently anaemic. Persistent B19 infection should be suspected in infants with congenital red-cell aplasia.

WHEN maternal rubella occurs during the first trimester of pregnancy, rubella virus can be detected in products of conception, in the fetus throughout pregnancy, and in the infant for several months after birth.¹Further, sera from children with the congenital rubella syndrome have been found to contain rubella neutralizing antibody in high titers.²Although these data clearly show that a state of immunologic tolerance does not exist, it is not known if the elevated levels of neutralizing antibody in the younger infant represent de novo synthesis of antibody by the infant or the transplacental transfer of maternal antibody. Following epidemic rubella occurring in the United States during the winter and spring of 1964, congenital rubella was observed in several centers. The neonatal syndrome consists of congenital heart disease, cataracts, hepatosplenomegaly, and thrombocytopenic purpura. It is the purpose of this report to present the significant clinical, hematologic, virologic, pathologic,

A significant depression in cell-mediated immunity, measured by phytohemagglutinin and mixed-lymphocyte-culture responsiveness was observed in 11 pregnant women. Specific cell-mediated immunity to rubella virus, measured by a ⁵¹Cr-release microassay, was also found to be diminished during pregnancy. The mean (± S.D.) specific immune release for 13 seropositive subjects during pregnancy was 4.3 ± 5.9 per cent as compared to a mean of 19.9 ± 0.9 per cent in 14 seropositive nonpregnant women. This impairment in specific cell-mediated immunity to rubella virus was shown to be transient because there was subsequent increase in immunity in each of four subjects studied post partum. Thus, these changes in cell-mediated immunity during pregnancy may contribute to the known increased severity of viral infections in the gravid state. (N Engl J Med 289:604–606, 1973)

Chronic fatigue syndrome (CFS) is a disorder of unknown etiology, consisting of prolonged, debilitating fatigue, and a multitude of symptoms including neurocognitive dysfunction, flu-like symptoms, myalgia, weakness, arthralgia, low-grade fever, sore throat, headache, sleep disturbances, and swelling and tenderness of lymph nodes. No effective treatment for CFS is known. The purpose of the study was to evaluate the efficacy of the reduced form of nicotinamide adenine dinucleotide (NADH) i.e., ENADA the stabilized oral absorbable form, in a randomized, double-blind, placebo-controlled crossover study in patients with CFS. Nicotinamide adenine dinucleotide is known to trigger energy production through ATP generation which may form the basis of its potential effects. Twenty-six eligible patients who fulfilled the Center for Disease Control and Prevention criteria for CFS completed the study. Medical history, physical examination, laboratory studies, and questionnaire were obtained at baseline, 4, 8, and 12 weeks. Subjects were randomly assigned to receive either 10 mg of NADH or placebo for a 4-week period. Following a 4-week washout period, subjects were crossed to the alternate regimen for a final 4-week period. No severe adverse effects were observed related to the study drug. Within this cohort of 26 patients, 8 of 26 (31%) responded favorably to NADH in contrast to 2 of 26 (8%) to placebo. Based upon these encouraging results we have decided to conduct an open-label study in a larger cohort of patients. Collectively, the results of this pilot study indicate that NADH may be a valuable adjunctive therapy in the management of the chronic fatigue syndrome and suggest that further clinical trials be performed to establish its efficacy in this clinically perplexing disorder.

Regulation of neural inflammation is considered as a vital therapeutic target in ischemic stroke. All-trans retinoic acid (atRA), a potent immune modulator, has raised interest in the field of stroke therapy. However, the immunological mechanisms for atRA-mediated neuroprotection remain elusive. The current study evaluated the impact of atRA on post-stroke neural inflammation and elucidated the mechanisms involved in the regulation of related neutrophil functions. atRA was prophylactically administered to mice 1 day before transient middle cerebral artery occlusion (tMCAO, 1 h) and repeated daily immediately after reperfusion for 3 days. Stroke outcomes, neutrophil polarization, and formation of neutrophil extracellular traps (NETs) in the stroke lesion were assessed. Neutrophil depletion was induced with anti-Ly6G antibodies. Primary neutrophil cultures were used to explore the mechanisms of atRA treatment. Prophylactic atRA treatment reduced infarct volumes and neurological deficits at 1 day after tMCAO. Post-stroke neural inflammation was attenuated and neutrophil accumulation in lesion was downregulated. atRA treatment skewed neutrophil toward N2 phenotype which facilitated its clearance by macrophage and inhibited NETs formation. The functions of neutrophil were indispensable in the protective effects of atRA and were associated with suppression to STAT1 signaling by atRA. Administration of atRA after stroke still provided efficient protection to cerebral ischemia. atRA displays potent therapeutic efficacy in ischemic stroke by attenuating neural inflammation. Treatment of atRA impeded neutrophil accumulation, favored N2 polarization, and forbade NETs formation in ischemic lesion. STAT1 signaling played a decisive role in the mechanisms of atRA-afforded regulation to neutrophil.