{'fraction_non_alphanumeric': 0.020046260601387818, 'fraction_numerical': 0.01156515034695451, 'mean_word_length': 5.831578947368421, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 1, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Development of metacyclic Leishmania promastigotes is associated with the increasing expression of GP65, the major surface antigen

Summary Using immunofluorescence techniques and flow microfluorometry analysis, we have demonstrated that the binding of a monoclonal antibody (VD5/ 25) produced against GP65, the major surface antigen of Leishmania braziliensis, increased on the surface of stationary‐phase promastigotes from all the New World Leishmania species causing mucocutaneous or cutaneous disease as compared with the log‐phase parasites. In addition, a sequential development of Leishmania amazonensis promastigotes from a non‐infective to an infective stage was demonstrated. Indeed, promastigotes in the stationary phase (days 6–7) were found to be far more infective than those in the logarithmic phase of growth (day 3) both in vitro for mouse peritoneal macrophages and in vivo for BALB/c mice. The intracellular survival and multiplication of L. amazonensis were significantly inhibited when infective promastigotes were treated with the VD5/25 monoclonal antibody. The increasing expression of GP65 on the promastigote surface may thus contribute to Leishmania infectivity. This seems to represent a characteristic mechanism applicable to all New World Leishmania species studied.