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Ashby (1919) the survival of cells derived from a blood group 0 donor and injected into a blood group A recipient were subjected to a mathematical analysis by Callender, Powell & Witts (1945) who found an average life span of 120 days. A similar result using an identical mathematical treatment was obtained by Jope (1946) who estimated the disappearance of sulphaemoglobin from the blood of subjects who had been in contact with trinitrotoluene immediately before the beginning of the experiment. The assumption implied in both methods is that the labelled cells have the same life span as the normal cells of the experimental subject. Shemin & Rittenberg (1946a, b) measured the rate of disappearance of 15N in the haemin isolated from subjects given isotopic glycine and showed that the average 'life span' of the haemoglobin molecule is about 120-125 days. A similar figure was obtained by Gray, Neuberger & Sneath (1950) who followed the "5N content of the stercobilin excreted by a normal subject fed isotopic glycine. The good agreement found between methods employing isotopic and non-isotopic labelling indicates that the haemoglobin in the circulating red cell of man is metabolically inert until the cell disintegrates. Isotope methods are more accurate than the other labelling techniques and give more detailed information about the distribution of life spans in a red cell population. The assumption which is made with all four methods that the rates of daily production and destruction are constant and equal, appears to be justified, at least in man, by the remarkable success which has been achieved in the quantitative interpretation of the data.Reliable data for few species other than man are available. Hawkins & Whipple (1938), working with bile fistula dogs, measured the interval between maximum regeneration of blood after bleeding or phenylhydrazine administration and the peak of increased excretion of bile pigments, and deduced from their results that the average life span of the dog red cell is about 125 days. Rittenberg & Bloch (1949), using the rate of incorporation of deuteriumlabelled acetate into the haem of the haemoglobin, estimated the average life span of the red cell of the rat to be about 100 days.The present paper is concerned with haemoglobin formation in the rabbit and the life span of the rabbit erythrocyte. Previous estimates of the latter vary within wide limits. Eaton & Damren (1930) found that after a haemorrhage rabbits show two or three reticulocyte responses, the second and third occurring about 8-17 days respectively after the first reticulocyte peak. They assumed that these later increases of reticulocytes are caused by the death of cells formed immediately after haemorrhage. It was deduced that the life span of these cells and presumably also of normal rabbit red cells is 8-9 days. Kurtz (1937) King & Gilchrist (1947). On this basis, provided that rabbit and human haemoglobin have the same mol. wt. and identical haem contents, a haemoglobin content of 100 % corresponds to 14-8 g.haem...

PLATE XCIV) IN 1951 Gledhill and Andrewes described a flterable agent which produced fatal hepatitis in mice. It was believed to have originated in P strain mice*, since it produced hepatitis in VSBS(VS) strain mice t when suspensions of viscera of P mice were passed blindly several times in VS mice. Later, Gledhill et al. (1952) showed that this agent consisted of two flbrable components ; a relatively labile one which was identified as Eperythrozoiin coccoides (Schilling, 1928, quoted by McCluskie andNiven, 1934) and a stable one which is now termed mouse hepatitis virus (MHV). It was shown that E . coccoides was carried by the P mice but not by VS mice and it was possible to separate E . coccoides from MHV by passage in VS mice with liver-spleen suspensions diluted to MHV was separated from contamination with E. coccoides by treating mice infected with the dual agent (MHV and E. coccoides mixture) with terramycin (oxytetracycline), to which E . coccoides is susceptible, or by filtration. It wm thus possible to maintain pure lines of both agents. The absence of E. coccoides in passes of MHV was confirmed by examination of blood 61ms and the absence of MHV in E. coccoides passages by histological studies. I n order to explain the original isolation it was considered probable that VS mice carry MHV which was liberated by passage in them of E. coccoides derived from P mice (Gledhill et al.). I n this paper the disease which MHV causes in normal and in E . codes-treated mice and the properties of the virus are discussed. M E T a O D SThe general methods conform to those already dmribed (Gledhill and Andrewes ; Gledhill et d.), except that undiluted liver-spleen suspensions are now atated to be 10-I dilutions. Batches of about 500 ml. of MHV were prepared by making 10 per cent. liver-spleen suspensions from VS mice infected with MHV 5-7 days previously. These suspensions were lightly centrifuged and aliquota were stored a t -7OoC. All references to E. wccoides-infected mice mean that they have been inoculated 2 or 3 days previously with a liver-spleen suspension containing E. wccoides in a dilution of 10-8.

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