Introduction: Exuberant inflammation during Pneumonia caused by Pneumocystis jiroveci strongly promotes pulmonary injury in HIV patients and suggested caused by Macrophage Inflammatory Protein 2- Alpha (MIP-2) as a strong chemoattractant.Aims: To understanding the potential roles of MIP-2 in the pulmonary injury in HIV patients.Methods: All complete coding sequences of human MIP-2 deposited inGenBank were downloadedand subjected for bioinformatics analysis.Results: Human MIP-2 lacks the highly conserved purine at position -3 but possess many features of the consensus sequence. The consensus polyadenylation signal was present in the hu-MIP-2a cDNA at position 1182-1187of the 3' untranslated region followed by a poly(A) beginning at nucleotide 1202. The cysteine alignment and the presence of non conserved amino acid were defining the properties of chemokines in case of what substances that could be attracted. The mechanism of lung injury perhaps does not caused by alteration of MIP-2 directly.

Keywords: MIP-2, HIV, lung injury, Pneumocystis jiroveci 

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