Figure 23–8 Dimorphism in the pathogenic fungus Histoplasma capsulatum. (A) At low temperature in the soil, H. capsulatum grows as a multicellular filamentous mold consisting of many individual cells connected together. (B) After it is inhaled into the lung of a mammal, the increase in temperature causes a switch to a yeast form consisting of small clumps of round cells. (C) A stained histologic section of a mouse lung infected with
H. capsulatum, showing a macrophage containing yeast forms of the pathogen. (A and B, courtesy of Sinem Beyhan and Anita Sil; C, courtesy of Davina Hocking Murray and Anita Sil.)
Figure 23–9 The complex life cycle of malaria parasites. (A) The sexual cycle of Plasmodium falciparum requires passage between a human host and an insect host (Movie 23.3). (B)–(D) Blood smears from people with malaria, showing three different forms of the parasite that appear in red blood cells: (B) ring stage; (C) schizont; and (D) gametocyte. (B–D, courtesy of the Centers for Disease Control, Division of Parasitic Diseases, DPDx.)
Plasmodium falciparum causes the most serious form of malaria and is the most intensively studied of the malaria-causing parasites. It exists in many distinct forms, and it requires both the human and mosquito hosts to complete its sexual cycle (Figure 23–9). Several of these forms are highly specialized to invade and replicate in specific tissues—the lining of the insect gut, the human liver, and the human red blood cell. Even within a single host cell type, the red blood cell, the Plasmodium parasite undergoes a complex sequence of developmental events, reflected in striking morphological changes (Figure 23–9B–D).
All Aspects of Viral Propagation Depend on Host Cell Machinery
Bacteria, fungal, and protozoan pathogens are living cells themselves. They use their own machinery for DNA replication, transcription, and translation, and, for the most part, they provide their own sources of metabolic energy. Viruses, by contrast, are the ultimate hitchhikers, carrying little more than information in the form of nucleic acid. Most clinically important human viruses have small genomes consisting of double-stranded DNA or single-stranded RNA (Table 23–1), and we now have complete genome sequences of almost all of them.
Viral genomes typically encode three types of protein: proteins for replicating the genome, proteins for packaging the genome and delivering it to more host cells, and proteins for modifying the structure or function of the host cell to enhance the replication of the virus (see Figure 7–62). In general, viral replication involves (1) entry into the host cell, (2) disassembly of the infectious virus particle, (3) replication of the viral genome, (4) transcription of viral genes and synthesis of viral proteins, (5) assembly of these viral components into progeny virus particles,
Figure 23–10 a simple viral life cycle. The hypothetical simple virus shown here consists of a small double-stranded DNA molecule that codes for only a single viral capsid protein. To reproduce, the viral genome must first enter a host cell, where it is replicated to produce multiple copies, which are transcribed and translated to produce the viral coat protein. The viral genomes can then assemble spontaneously with the coat protein to form a new virus particle, which escapes from the host cell. No known virus is this simple.
and (6) release of progeny virions (Figure 23–10). A single virus particle (a virion) that infects a single host cell can produce thousands of progeny.